https://tncentral.ncc.unesp.br/TnPedia/index.php?title=General_Information/ClpX,_ClpP,_and_Lon&feed=atom&action=historyGeneral Information/ClpX, ClpP, and Lon - Revision history2024-03-28T13:06:56ZRevision history for this page on the wikiMediaWiki 1.34.0https://tncentral.ncc.unesp.br/TnPedia/index.php?title=General_Information/ClpX,_ClpP,_and_Lon&diff=1314&oldid=prevTnCentral at 17:42, 22 June 20202020-06-22T17:42:25Z<p></p>
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<td colspan="2" style="background-color: #fff; color: #222; text-align: center;">Revision as of 17:42, 22 June 2020</td>
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<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>====SOS system, RecA, RecBC====</div></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>====SOS system, RecA, RecBC====</div></td></tr>
<tr><td class='diff-marker'>−</td><td style="color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div>The third class of host factor includes host cell systems which act to limit DNA damage and maintain chromosome integrity. Studies with IS''10'' (see <ref><nowiki><pubmed>8556869</pubmed></nowiki></ref>) and IS''1''<ref><nowiki><pubmed>7932694</pubmed></nowiki></ref> have demonstrated that high levels of Tpase in the presence of suitable terminal IRs lead to induction of the host [[wikipedia:SOS_response|SOS system]]. As discussed previously<ref><nowiki><pubmed>9729608</pubmed></nowiki></ref>, some controversy still exists concerning the role of [[wikipedia:RecA|RecA]] in Tn''5'' (IS''50'') transposition<ref<del class="diffchange diffchange-inline">><nowiki</del>><pubmed>1648004</pubmed></nowiki></ref><ref<del class="diffchange diffchange-inline">><nowiki</del>><pubmed>1655708</pubmed></nowiki></ref><ref<del class="diffchange diffchange-inline">><nowiki</del>><pubmed>1657870</pubmed></nowiki></ref>. [https://biochem.wisc.edu/emeritus/reznikoff/cv Reznikoff] and colleagues have provided genetic evidence that transposition is inhibited by induction of the [[wikipedia:SOS_response|SOS system]] in a manner which does not require the proteolytic activity of [[wikipedia:RecA|RecA]]<ref<del class="diffchange diffchange-inline">><nowiki><pubmed>1657870<</del>/<del class="diffchange diffchange-inline">pubmed></nowiki></ref</del>>. On the other hand, Tessman and collaborators<ref<del class="diffchange diffchange-inline">><nowiki><pubmed>1648004<</del>/<del class="diffchange diffchange-inline">pubmed</del>><<del class="diffchange diffchange-inline">/nowiki></</del>ref<del class="diffchange diffchange-inline">><ref><nowiki><pubmed>1655708<</del>/<del class="diffchange diffchange-inline">pubmed></nowiki></ref</del>><ref><nowiki><pubmed>1328165</pubmed></nowiki></ref> using a different transposition assay have found that constitutive SOS conditions actually enhance Tn''5'' transposition. Moreover, using yet another assay system, Ahmed<ref name=":0"><pubmed>3025455</pubmed></nowiki></ref> has concluded that intermolecular transposition of Tn''5'' is stimulated by RecA. Further investigation is clearly required to understand these apparently incompatible results.</div></td><td class='diff-marker'>+</td><td style="color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div>The third class of host factor includes host cell systems which act to limit DNA damage and maintain chromosome integrity. Studies with IS''10'' (see <ref><nowiki><pubmed>8556869</pubmed></nowiki></ref>) and IS''1''<ref><nowiki><pubmed>7932694</pubmed></nowiki></ref> have demonstrated that high levels of Tpase in the presence of suitable terminal IRs lead to induction of the host [[wikipedia:SOS_response|SOS system]]. As discussed previously<ref><nowiki><pubmed>9729608</pubmed></nowiki></ref>, some controversy still exists concerning the role of [[wikipedia:RecA|RecA]] in Tn''5'' (IS''50'') transposition<ref <ins class="diffchange diffchange-inline">name=":1"</ins>><pubmed>1648004</pubmed></nowiki></ref><ref <ins class="diffchange diffchange-inline">name=":2"</ins>><pubmed>1655708</pubmed></nowiki></ref><ref <ins class="diffchange diffchange-inline">name=":3"</ins>><pubmed>1657870</pubmed></nowiki></ref>. [https://biochem.wisc.edu/emeritus/reznikoff/cv Reznikoff] and colleagues have provided genetic evidence that transposition is inhibited by induction of the [[wikipedia:SOS_response|SOS system]] in a manner which does not require the proteolytic activity of [[wikipedia:RecA|RecA]]<ref <ins class="diffchange diffchange-inline">name=":3" </ins>/>. On the other hand, Tessman and collaborators<ref <ins class="diffchange diffchange-inline">name=":1" </ins>/><ref <ins class="diffchange diffchange-inline">name=":2" </ins>/><ref><nowiki><pubmed>1328165</pubmed></nowiki></ref> using a different transposition assay have found that constitutive SOS conditions actually enhance Tn''5'' transposition. Moreover, using yet another assay system, Ahmed<ref name=":0"><pubmed>3025455</pubmed></nowiki></ref> has concluded that intermolecular transposition of Tn''5'' is stimulated by RecA. Further investigation is clearly required to understand these apparently incompatible results.</div></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>Ahmed has also concluded that intermolecular transposition of the IS''1''-based transposon, Tn''9'', behaves in a similar way to that of Tn''5'' with respect to the ''[[wikipedia:RecA|recA]]'' allele<ref name=":0" />. In contrast, however, the frequency of adjacent deletions mediated by IS''1'' was significantly increased in the absence of [[wikipedia:RecA|RecA]]. This has received some independent support using a physical assay where it was shown that deletion products accumulate in a ''recA'' but not in a wildtype host. Moreover, like IS''1'' induction of the [[wikipedia:SOS_response|SOS system]], accumulation of such adjacent deletions was dependent on ''recBC'' (Zablweska et al., unpublished observations). The ''recBC'' genes are also implicated in the behavior of transposons such as Tn''10'' and Tn''5''<ref name=":0" /> where they affect precise and imprecise excision in a process independent of transposition per se. This is more pronounced with composite transposons in which the component insertion sequences IS''10'' and IS''50'' are present as inverted repeats, and is stimulated when the transposon is carried by a transfer-proficient conjugative plasmid. It seems probable that such excisions occur by a process involving replication fork slippage (see <ref><nowiki><pubmed>10844241</pubmed></nowiki></ref><ref><nowiki><pubmed>10715006</pubmed></nowiki></ref> for further discussion).</div></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>Ahmed has also concluded that intermolecular transposition of the IS''1''-based transposon, Tn''9'', behaves in a similar way to that of Tn''5'' with respect to the ''[[wikipedia:RecA|recA]]'' allele<ref name=":0" />. In contrast, however, the frequency of adjacent deletions mediated by IS''1'' was significantly increased in the absence of [[wikipedia:RecA|RecA]]. This has received some independent support using a physical assay where it was shown that deletion products accumulate in a ''recA'' but not in a wildtype host. Moreover, like IS''1'' induction of the [[wikipedia:SOS_response|SOS system]], accumulation of such adjacent deletions was dependent on ''recBC'' (Zablweska et al., unpublished observations). The ''recBC'' genes are also implicated in the behavior of transposons such as Tn''10'' and Tn''5''<ref name=":0" /> where they affect precise and imprecise excision in a process independent of transposition per se. This is more pronounced with composite transposons in which the component insertion sequences IS''10'' and IS''50'' are present as inverted repeats, and is stimulated when the transposon is carried by a transfer-proficient conjugative plasmid. It seems probable that such excisions occur by a process involving replication fork slippage (see <ref><nowiki><pubmed>10844241</pubmed></nowiki></ref><ref><nowiki><pubmed>10715006</pubmed></nowiki></ref> for further discussion).</div></td></tr>
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<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>====Dam methylase====</div></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>====Dam methylase====</div></td></tr>
<tr><td class='diff-marker'>−</td><td style="color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div>Another host function, the [[wikipedia:DNA_adenine_methylase|Dam DNA methylase]] can be important in modulating both Tpase expression and activity. IS''10'', IS''50'' and IS''903'' all carry methylation sites (GATC) in the transposase promoter regions and in each case, promoter activity is increased in a dam-host<ref<del class="diffchange diffchange-inline">><nowiki</del>><pubmed>3000598</pubmed></nowiki></ref><ref><nowiki><pubmed>2451025</pubmed></nowiki></ref>. Additional evidence has been presented that the methylation status of GATC sites within the terminal inverted repeats also modulates the activity of these ends<ref<del class="diffchange diffchange-inline">><nowiki><pubmed>3000598</pubmed><</del>/<del class="diffchange diffchange-inline">nowiki></ref</del>>. For IS''50'', this can now be understood in terms of steric interference in the transposase active site, as recently revealed by the determination of the crystal structure of a synpatic complex including its Tpase and a pair of precleaved transposon ends<ref><nowiki><pubmed>10207011</pubmed></nowiki></ref>. Similar methylation sites have been previously observed in IS''3'', IS''4'', and IS''5''. A survey of the elements included in the data base has shown that most groups or families contain members which have GATC sites within the first 50 bp of one or both extremities. The [[IS Families/IS3 family|IS''3'']]'','' [[IS Families/IS5 and related IS1182 families|IS''5'']] and [[IS Families/IS256 family|IS''256'']] families include the most members carrying such sites. Except for [[IS Families/IS3 family|IS''3'']] itself where strong stimulation of transposition has been observed in a dam-host, in most of these cases the biological relevance of these sites is unknown. Moreover, it should be pointed out that the probability that any 100 bp DNA sequence carries the GATC tetranucleotide is about 40%. The role of Dam methylation in IS''10'' and IS''50'' transposition is described in detail in the appropriate sections dealing with these elements.</div></td><td class='diff-marker'>+</td><td style="color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div>Another host function, the [[wikipedia:DNA_adenine_methylase|Dam DNA methylase]] can be important in modulating both Tpase expression and activity. IS''10'', IS''50'' and IS''903'' all carry methylation sites (GATC) in the transposase promoter regions and in each case, promoter activity is increased in a dam-host<ref <ins class="diffchange diffchange-inline">name=":4"</ins>><pubmed>3000598</pubmed></nowiki></ref><ref><nowiki><pubmed>2451025</pubmed></nowiki></ref>. Additional evidence has been presented that the methylation status of GATC sites within the terminal inverted repeats also modulates the activity of these ends<ref <ins class="diffchange diffchange-inline">name=":4" </ins>/>. For IS''50'', this can now be understood in terms of steric interference in the transposase active site, as recently revealed by the determination of the crystal structure of a synpatic complex including its Tpase and a pair of precleaved transposon ends<ref><nowiki><pubmed>10207011</pubmed></nowiki></ref>. Similar methylation sites have been previously observed in IS''3'', IS''4'', and IS''5''. A survey of the elements included in the data base has shown that most groups or families contain members which have GATC sites within the first 50 bp of one or both extremities. The [[IS Families/IS3 family|IS''3'']]'','' [[IS Families/IS5 and related IS1182 families|IS''5'']] and [[IS Families/IS256 family|IS''256'']] families include the most members carrying such sites. Except for [[IS Families/IS3 family|IS''3'']] itself where strong stimulation of transposition has been observed in a dam-host, in most of these cases the biological relevance of these sites is unknown. Moreover, it should be pointed out that the probability that any 100 bp DNA sequence carries the GATC tetranucleotide is about 40%. The role of Dam methylation in IS''10'' and IS''50'' transposition is described in detail in the appropriate sections dealing with these elements.</div></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>====Metabolic control elements====</div></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>====Metabolic control elements====</div></td></tr>
</table>TnCentralhttps://tncentral.ncc.unesp.br/TnPedia/index.php?title=General_Information/ClpX,_ClpP,_and_Lon&diff=1293&oldid=prevTnCentral at 13:26, 15 June 20202020-06-15T13:26:53Z<p></p>
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<td colspan="2" style="background-color: #fff; color: #222; text-align: center;">Revision as of 13:26, 15 June 2020</td>
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<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>====SOS system, RecA, RecBC====</div></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>====SOS system, RecA, RecBC====</div></td></tr>
<tr><td class='diff-marker'>−</td><td style="color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div>The third class of host factor includes host cell systems which act to limit DNA damage and maintain chromosome integrity. Studies with IS''10'' (see <ref><nowiki><pubmed>8556869</pubmed></nowiki></ref>) and IS''1''<ref><nowiki><pubmed>7932694</pubmed></nowiki></ref> have demonstrated that high levels of Tpase in the presence of suitable terminal IRs lead to induction of the host [[wikipedia:SOS_response|SOS system]]. As discussed previously<ref><nowiki><pubmed>9729608</pubmed></nowiki></ref>, some controversy still exists concerning the role of [[wikipedia:RecA|RecA]] in Tn''5'' (IS''50'') transposition<ref><nowiki><pubmed>1648004</pubmed></nowiki></ref><ref><nowiki><pubmed>1655708</pubmed></nowiki></ref><ref><nowiki><pubmed>1657870</pubmed></nowiki></ref>. [https://biochem.wisc.edu/emeritus/reznikoff/cv Reznikoff] and colleagues have provided genetic evidence that transposition is inhibited by induction of the [[wikipedia:SOS_response|SOS system]] in a manner which does not require the proteolytic activity of [[wikipedia:RecA|RecA]]<ref><nowiki><pubmed>1657870</pubmed></nowiki></ref>. On the other hand, Tessman and collaborators<ref><nowiki><pubmed>1648004</pubmed></nowiki></ref><ref><nowiki><pubmed>1655708</pubmed></nowiki></ref><ref><nowiki><pubmed>1328165</pubmed></nowiki></ref> using a different transposition assay have found that constitutive SOS conditions actually enhance Tn''5'' transposition. Moreover, using yet another assay system, Ahmed<ref<del class="diffchange diffchange-inline">><nowiki</del>><pubmed>3025455</pubmed></nowiki></ref> has concluded that intermolecular transposition of Tn''5'' is stimulated by RecA. Further investigation is clearly required to understand these apparently incompatible results.</div></td><td class='diff-marker'>+</td><td style="color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div>The third class of host factor includes host cell systems which act to limit DNA damage and maintain chromosome integrity. Studies with IS''10'' (see <ref><nowiki><pubmed>8556869</pubmed></nowiki></ref>) and IS''1''<ref><nowiki><pubmed>7932694</pubmed></nowiki></ref> have demonstrated that high levels of Tpase in the presence of suitable terminal IRs lead to induction of the host [[wikipedia:SOS_response|SOS system]]. As discussed previously<ref><nowiki><pubmed>9729608</pubmed></nowiki></ref>, some controversy still exists concerning the role of [[wikipedia:RecA|RecA]] in Tn''5'' (IS''50'') transposition<ref><nowiki><pubmed>1648004</pubmed></nowiki></ref><ref><nowiki><pubmed>1655708</pubmed></nowiki></ref><ref><nowiki><pubmed>1657870</pubmed></nowiki></ref>. [https://biochem.wisc.edu/emeritus/reznikoff/cv Reznikoff] and colleagues have provided genetic evidence that transposition is inhibited by induction of the [[wikipedia:SOS_response|SOS system]] in a manner which does not require the proteolytic activity of [[wikipedia:RecA|RecA]]<ref><nowiki><pubmed>1657870</pubmed></nowiki></ref>. On the other hand, Tessman and collaborators<ref><nowiki><pubmed>1648004</pubmed></nowiki></ref><ref><nowiki><pubmed>1655708</pubmed></nowiki></ref><ref><nowiki><pubmed>1328165</pubmed></nowiki></ref> using a different transposition assay have found that constitutive SOS conditions actually enhance Tn''5'' transposition. Moreover, using yet another assay system, Ahmed<ref <ins class="diffchange diffchange-inline">name=":0"</ins>><pubmed>3025455</pubmed></nowiki></ref> has concluded that intermolecular transposition of Tn''5'' is stimulated by RecA. Further investigation is clearly required to understand these apparently incompatible results.</div></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"></td></tr>
<tr><td class='diff-marker'>−</td><td style="color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div>Ahmed has also concluded that intermolecular transposition of the IS''1''-based transposon, Tn''9'', behaves in a similar way to that of Tn''5'' with respect to the ''[[wikipedia:RecA|recA]]'' allele<ref<del class="diffchange diffchange-inline">><nowiki><pubmed>3025455</pubmed><</del>/<del class="diffchange diffchange-inline">nowiki></ref</del>>. In contrast, however, the frequency of adjacent deletions mediated by IS''1'' was significantly increased in the absence of [[wikipedia:RecA|RecA]]. This has received some independent support using a physical assay where it was shown that deletion products accumulate in a ''recA'' but not in a wildtype host. Moreover, like IS''1'' induction of the [[wikipedia:SOS_response|SOS system]], accumulation of such adjacent deletions was dependent on ''recBC'' (Zablweska et al., unpublished observations). The ''recBC'' genes are also implicated in the behavior of transposons such as Tn''10'' and Tn''5''<ref<del class="diffchange diffchange-inline">><nowiki><pubmed>3025455<</del>/<del class="diffchange diffchange-inline">pubmed></nowiki></ref><ref><nowiki><pubmed>6322169</pubmed></nowiki></ref</del>> where they affect precise and imprecise excision in a process independent of transposition per se. This is more pronounced with composite transposons in which the component insertion sequences IS''10'' and IS''50'' are present as inverted repeats, and is stimulated when the transposon is carried by a transfer-proficient conjugative plasmid. It seems probable that such excisions occur by a process involving replication fork slippage (see <ref><nowiki><pubmed>10844241</pubmed></nowiki></ref><ref><nowiki><pubmed>10715006</pubmed></nowiki></ref> for further discussion).</div></td><td class='diff-marker'>+</td><td style="color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div>Ahmed has also concluded that intermolecular transposition of the IS''1''-based transposon, Tn''9'', behaves in a similar way to that of Tn''5'' with respect to the ''[[wikipedia:RecA|recA]]'' allele<ref <ins class="diffchange diffchange-inline">name=":0" </ins>/>. In contrast, however, the frequency of adjacent deletions mediated by IS''1'' was significantly increased in the absence of [[wikipedia:RecA|RecA]]. This has received some independent support using a physical assay where it was shown that deletion products accumulate in a ''recA'' but not in a wildtype host. Moreover, like IS''1'' induction of the [[wikipedia:SOS_response|SOS system]], accumulation of such adjacent deletions was dependent on ''recBC'' (Zablweska et al., unpublished observations). The ''recBC'' genes are also implicated in the behavior of transposons such as Tn''10'' and Tn''5''<ref <ins class="diffchange diffchange-inline">name=":0" </ins>/> where they affect precise and imprecise excision in a process independent of transposition per se. This is more pronounced with composite transposons in which the component insertion sequences IS''10'' and IS''50'' are present as inverted repeats, and is stimulated when the transposon is carried by a transfer-proficient conjugative plasmid. It seems probable that such excisions occur by a process involving replication fork slippage (see <ref><nowiki><pubmed>10844241</pubmed></nowiki></ref><ref><nowiki><pubmed>10715006</pubmed></nowiki></ref> for further discussion).</div></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>====PolI and gyrase====</div></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>====PolI and gyrase====</div></td></tr>
</table>TnCentralhttps://tncentral.ncc.unesp.br/TnPedia/index.php?title=General_Information/ClpX,_ClpP,_and_Lon&diff=1105&oldid=prevTnCentral at 19:06, 3 June 20202020-06-03T19:06:07Z<p></p>
<table class="diff diff-contentalign-left" data-mw="interface">
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<td colspan="2" style="background-color: #fff; color: #222; text-align: center;">← Older revision</td>
<td colspan="2" style="background-color: #fff; color: #222; text-align: center;">Revision as of 19:06, 3 June 2020</td>
</tr><tr><td colspan="2" class="diff-lineno" id="mw-diff-left-l1" >Line 1:</td>
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<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>====General====</div></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>====General====</div></td></tr>
<tr><td class='diff-marker'>−</td><td style="color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div>'''<big>C</big>'''ertain factors involved in protein "management" such as ClpX, ClpP, and Lon have been implicated in transposition. ClpX is essential for Mu growth<ref><nowiki><pubmed>8022280</pubmed></nowiki></ref> where it is required for disassembling the transposase-DNA complex or the transpososome strand transfer complex in preparation for the assembly of a replication complex<ref><nowiki><pubmed>8631314</pubmed></nowiki></ref><ref><nowiki><pubmed>7557391</pubmed></nowiki></ref>. Recognition of Mu transposase, pA, by ClpX requires the terminal 10 amino acids of pA<ref><nowiki><pubmed>9203582</pubmed></nowiki></ref>. Together with ClpP, ClpX also plays a role in proteolysis of the Mu repressor<ref><nowiki><pubmed>8617219</pubmed></nowiki></ref><ref><nowiki><pubmed>9299335</pubmed></nowiki></ref>. The Lon protease is implicated in proteolysis of the IS''903'' transposase<ref><nowiki><pubmed>2161528</pubmed></nowiki></ref>.</div></td><td class='diff-marker'>+</td><td style="color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div>'''<big>C</big>'''ertain factors involved in protein "management" such as <ins class="diffchange diffchange-inline">[[wikipedia:</ins>ClpX<ins class="diffchange diffchange-inline">|ClpX]]</ins>, <ins class="diffchange diffchange-inline">[[wikipedia:Clp_protease_family|</ins>ClpP<ins class="diffchange diffchange-inline">]]</ins>, and <ins class="diffchange diffchange-inline">[[wikipedia:Lon_protease_family|</ins>Lon<ins class="diffchange diffchange-inline">]] </ins>have been implicated in transposition. ClpX is essential for <ins class="diffchange diffchange-inline">[[wikipedia:Bacteriophage_Mu|bacteriophage </ins>Mu<ins class="diffchange diffchange-inline">]] </ins>growth<ref><nowiki><pubmed>8022280</pubmed></nowiki></ref> where it is required for disassembling the transposase-DNA complex or the transpososome strand transfer complex in preparation for the assembly of a replication complex<ref><nowiki><pubmed>8631314</pubmed></nowiki></ref><ref><nowiki><pubmed>7557391</pubmed></nowiki></ref>. Recognition of Mu transposase, pA, by ClpX requires the terminal 10 amino acids of pA<ref><nowiki><pubmed>9203582</pubmed></nowiki></ref>. Together with ClpP, ClpX also plays a role in proteolysis of the Mu repressor<ref><nowiki><pubmed>8617219</pubmed></nowiki></ref><ref><nowiki><pubmed>9299335</pubmed></nowiki></ref>. The Lon protease is implicated in proteolysis of the IS''903'' transposase<ref><nowiki><pubmed>2161528</pubmed></nowiki></ref>.</div></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>At present the involvement of these proteins in the transposition of other elements has not been well documented.</div></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>At present the involvement of these proteins in the transposition of other elements has not been well documented.</div></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>====SOS system, RecA, RecBC====</div></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>====SOS system, RecA, RecBC====</div></td></tr>
<tr><td class='diff-marker'>−</td><td style="color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div>The third class of host factor includes host cell systems which act to limit DNA damage and maintain chromosome integrity. Studies with IS''10'' (see <ref><nowiki><pubmed>8556869</pubmed></nowiki></ref>) and IS''1''<ref><nowiki><pubmed>7932694</pubmed></nowiki></ref> have demonstrated that high levels of Tpase in the presence of suitable terminal IRs lead to induction of the host [[wikipedia:SOS_response|SOS system]]. As discussed previously<ref><nowiki><pubmed>9729608</pubmed></nowiki></ref>, some controversy still exists concerning the role of RecA in Tn''5'' (IS''50'') transposition<ref><nowiki><pubmed>1648004</pubmed></nowiki></ref><ref><nowiki><pubmed>1655708</pubmed></nowiki></ref><ref><nowiki><pubmed>1657870</pubmed></nowiki></ref>. Reznikoff and colleagues have provided genetic evidence that transposition is inhibited by induction of the SOS system in a manner which does not require the proteolytic activity of RecA<ref><nowiki><pubmed>1657870</pubmed></nowiki></ref>. On the other hand, Tessman and collaborators<ref><nowiki><pubmed>1648004</pubmed></nowiki></ref><ref><nowiki><pubmed>1655708</pubmed></nowiki></ref><ref><nowiki><pubmed>1328165</pubmed></nowiki></ref> using a different transposition assay have found that constitutive SOS conditions actually enhance Tn''5'' transposition. Moreover, using yet another assay system, Ahmed<ref><nowiki><pubmed>3025455</pubmed></nowiki></ref> has concluded that intermolecular transposition of Tn''5'' is stimulated by RecA. Further investigation is clearly required to understand these apparently incompatible results.</div></td><td class='diff-marker'>+</td><td style="color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div>The third class of host factor includes host cell systems which act to limit DNA damage and maintain chromosome integrity. Studies with IS''10'' (see <ref><nowiki><pubmed>8556869</pubmed></nowiki></ref>) and IS''1''<ref><nowiki><pubmed>7932694</pubmed></nowiki></ref> have demonstrated that high levels of Tpase in the presence of suitable terminal IRs lead to induction of the host [[wikipedia:SOS_response|SOS system]]. As discussed previously<ref><nowiki><pubmed>9729608</pubmed></nowiki></ref>, some controversy still exists concerning the role of <ins class="diffchange diffchange-inline">[[wikipedia:</ins>RecA<ins class="diffchange diffchange-inline">|RecA]] </ins>in Tn''5'' (IS''50'') transposition<ref><nowiki><pubmed>1648004</pubmed></nowiki></ref><ref><nowiki><pubmed>1655708</pubmed></nowiki></ref><ref><nowiki><pubmed>1657870</pubmed></nowiki></ref>. <ins class="diffchange diffchange-inline">[https://biochem.wisc.edu/emeritus/reznikoff/cv </ins>Reznikoff<ins class="diffchange diffchange-inline">] </ins>and colleagues have provided genetic evidence that transposition is inhibited by induction of the <ins class="diffchange diffchange-inline">[[wikipedia:SOS_response|</ins>SOS system<ins class="diffchange diffchange-inline">]] </ins>in a manner which does not require the proteolytic activity of <ins class="diffchange diffchange-inline">[[wikipedia:RecA|</ins>RecA<ins class="diffchange diffchange-inline">]]</ins><ref><nowiki><pubmed>1657870</pubmed></nowiki></ref>. On the other hand, Tessman and collaborators<ref><nowiki><pubmed>1648004</pubmed></nowiki></ref><ref><nowiki><pubmed>1655708</pubmed></nowiki></ref><ref><nowiki><pubmed>1328165</pubmed></nowiki></ref> using a different transposition assay have found that constitutive SOS conditions actually enhance Tn''5'' transposition. Moreover, using yet another assay system, Ahmed<ref><nowiki><pubmed>3025455</pubmed></nowiki></ref> has concluded that intermolecular transposition of Tn''5'' is stimulated by RecA. Further investigation is clearly required to understand these apparently incompatible results.</div></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"></td></tr>
<tr><td class='diff-marker'>−</td><td style="color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div>Ahmed has also concluded that intermolecular transposition of the IS''1''-based transposon, Tn''9'', behaves in a similar way to that of Tn''5'' with respect to the recA allele<ref><nowiki><pubmed>3025455</pubmed></nowiki></ref>. In contrast, however, the frequency of adjacent deletions mediated by IS''1'' was significantly increased in the absence of RecA. This has received some independent support using a physical assay where it was shown that deletion products accumulate in a recA but not in a wildtype host. Moreover, like IS''1'' induction of the [[wikipedia:SOS_response|SOS system]], accumulation of such adjacent deletions was dependent on ''recBC'' (Zablweska et al., unpublished observations). The ''recBC'' genes are also implicated in the behavior of transposons such as Tn''10'' and Tn''5''<ref><nowiki><pubmed>3025455</pubmed></nowiki></ref><ref><nowiki><pubmed>6322169</pubmed></nowiki></ref> where they affect precise and imprecise excision in a process independent of transposition per se. This is more pronounced with composite transposons in which the component insertion sequences IS''10'' and IS''50'' are present as inverted repeats, and is stimulated when the transposon is carried by a transfer-proficient conjugative plasmid. It seems probable that such excisions occur by a process involving replication fork slippage (see <ref><nowiki><pubmed>10844241</pubmed></nowiki></ref><ref><nowiki><pubmed>10715006</pubmed></nowiki></ref> for further discussion).</div></td><td class='diff-marker'>+</td><td style="color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div>Ahmed has also concluded that intermolecular transposition of the IS''1''-based transposon, Tn''9'', behaves in a similar way to that of Tn''5'' with respect to the <ins class="diffchange diffchange-inline">''[[wikipedia:RecA|</ins>recA<ins class="diffchange diffchange-inline">]]'' </ins>allele<ref><nowiki><pubmed>3025455</pubmed></nowiki></ref>. In contrast, however, the frequency of adjacent deletions mediated by IS''1'' was significantly increased in the absence of <ins class="diffchange diffchange-inline">[[wikipedia:RecA|</ins>RecA<ins class="diffchange diffchange-inline">]]</ins>. This has received some independent support using a physical assay where it was shown that deletion products accumulate in a <ins class="diffchange diffchange-inline">''</ins>recA<ins class="diffchange diffchange-inline">'' </ins>but not in a wildtype host. Moreover, like IS''1'' induction of the [[wikipedia:SOS_response|SOS system]], accumulation of such adjacent deletions was dependent on ''recBC'' (Zablweska et al., unpublished observations). The ''recBC'' genes are also implicated in the behavior of transposons such as Tn''10'' and Tn''5''<ref><nowiki><pubmed>3025455</pubmed></nowiki></ref><ref><nowiki><pubmed>6322169</pubmed></nowiki></ref> where they affect precise and imprecise excision in a process independent of transposition per se. This is more pronounced with composite transposons in which the component insertion sequences IS''10'' and IS''50'' are present as inverted repeats, and is stimulated when the transposon is carried by a transfer-proficient conjugative plasmid. It seems probable that such excisions occur by a process involving replication fork slippage (see <ref><nowiki><pubmed>10844241</pubmed></nowiki></ref><ref><nowiki><pubmed>10715006</pubmed></nowiki></ref> for further discussion).</div></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>====PolI and gyrase====</div></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>====PolI and gyrase====</div></td></tr>
<tr><td class='diff-marker'>−</td><td style="color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div>Both DNA polymerase I <ref><nowiki><pubmed>6267432</pubmed></nowiki></ref><ref><nowiki><pubmed>6288966</pubmed></nowiki></ref><ref><nowiki><pubmed>3030303</pubmed></nowiki></ref> and DNA gyrase<ref><nowiki><pubmed>6290084</pubmed></nowiki></ref><ref><nowiki><pubmed>6265907</pubmed></nowiki></ref> are implicated in the transposition of Tn''5''. While the effect of gyrase may reflect a requirement for optimal levels of supercoiling, the role of PolI remains a matter of speculation. It may be involved in DNA synthesis necessary to repair the single strand gaps resulting from staggered cleavage of the target and which gives rise to the DRs. DNA gyrase has also been shown to be important in transposition of [[wikipedia:Bacteriophage_Mu|bacteriophage Mu]]<ref><nowiki><pubmed>7592347</pubmed></nowiki></ref><ref><nowiki><pubmed>8930913</pubmed></nowiki></ref>.</div></td><td class='diff-marker'>+</td><td style="color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div>Both <ins class="diffchange diffchange-inline">[[wikipedia:DNA_polymerase_I|</ins>DNA polymerase I<ins class="diffchange diffchange-inline">]] </ins><ref><nowiki><pubmed>6267432</pubmed></nowiki></ref><ref><nowiki><pubmed>6288966</pubmed></nowiki></ref><ref><nowiki><pubmed>3030303</pubmed></nowiki></ref> and <ins class="diffchange diffchange-inline">[[wikipedia:DNA_gyrase|</ins>DNA gyrase<ins class="diffchange diffchange-inline">]]</ins><ref><nowiki><pubmed>6290084</pubmed></nowiki></ref><ref><nowiki><pubmed>6265907</pubmed></nowiki></ref> are implicated in the transposition of Tn''5''. While the effect of gyrase may reflect a requirement for optimal levels of supercoiling, the role of PolI remains a matter of speculation. It may be involved in DNA synthesis necessary to repair the single strand gaps resulting from staggered cleavage of the target and which gives rise to the DRs. DNA gyrase has also been shown to be important in transposition of [[wikipedia:Bacteriophage_Mu|bacteriophage Mu]]<ref><nowiki><pubmed>7592347</pubmed></nowiki></ref><ref><nowiki><pubmed>8930913</pubmed></nowiki></ref>.</div></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>====Dam methylase====</div></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>====Dam methylase====</div></td></tr>
<tr><td class='diff-marker'>−</td><td style="color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div>Another host function, the Dam DNA methylase can be important in modulating both Tpase expression and activity. IS''10'', IS''50'' and IS''903'' all carry methylation sites (GATC) in the transposase promoter regions and in each case, promoter activity is increased in a dam-host<ref><nowiki><pubmed>3000598</pubmed></nowiki></ref><ref><nowiki><pubmed>2451025</pubmed></nowiki></ref>. Additional evidence has been presented that the methylation status of GATC sites within the terminal inverted repeats also modulates the activity of these ends<ref><nowiki><pubmed>3000598</pubmed></nowiki></ref>. For IS''50'', this can now be understood in terms of steric interference in the transposase active site, as recently revealed by the determination of the crystal structure of a synpatic complex including its Tpase and a pair of precleaved transposon ends<ref><nowiki><pubmed>10207011</pubmed></nowiki></ref>. Similar methylation sites have been previously observed in IS''3'', IS''4'', and IS''5''. A survey of the elements included in the data base has shown that most groups or families contain members which have GATC sites within the first 50 bp of one or both extremities. The IS''3,'' IS''5'' and IS''256'' families include the most members carrying such sites. Except for IS''3'' itself where strong stimulation of transposition has been observed in a dam-host, in most of these cases the biological relevance of these sites is unknown. Moreover, it should be pointed out that the probability that any 100 bp DNA sequence carries the GATC tetranucleotide is about 40%. The role of Dam methylation in IS''10'' and IS''50'' transposition is described in detail in the appropriate sections dealing with these elements.</div></td><td class='diff-marker'>+</td><td style="color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div>Another host function, the <ins class="diffchange diffchange-inline">[[wikipedia:DNA_adenine_methylase|</ins>Dam DNA methylase<ins class="diffchange diffchange-inline">]] </ins>can be important in modulating both Tpase expression and activity. IS''10'', IS''50'' and IS''903'' all carry methylation sites (GATC) in the transposase promoter regions and in each case, promoter activity is increased in a dam-host<ref><nowiki><pubmed>3000598</pubmed></nowiki></ref><ref><nowiki><pubmed>2451025</pubmed></nowiki></ref>. Additional evidence has been presented that the methylation status of GATC sites within the terminal inverted repeats also modulates the activity of these ends<ref><nowiki><pubmed>3000598</pubmed></nowiki></ref>. For IS''50'', this can now be understood in terms of steric interference in the transposase active site, as recently revealed by the determination of the crystal structure of a synpatic complex including its Tpase and a pair of precleaved transposon ends<ref><nowiki><pubmed>10207011</pubmed></nowiki></ref>. Similar methylation sites have been previously observed in IS''3'', IS''4'', and IS''5''. A survey of the elements included in the data base has shown that most groups or families contain members which have GATC sites within the first 50 bp of one or both extremities. The <ins class="diffchange diffchange-inline">[[IS Families/IS3 family|</ins>IS''3<ins class="diffchange diffchange-inline">'']]''</ins>,'' <ins class="diffchange diffchange-inline">[[IS Families/IS5 and related IS1182 families|</ins>IS''5''<ins class="diffchange diffchange-inline">]] </ins>and <ins class="diffchange diffchange-inline">[[IS Families/IS256 family|</ins>IS''256''<ins class="diffchange diffchange-inline">]] </ins>families include the most members carrying such sites. Except for <ins class="diffchange diffchange-inline">[[IS Families/IS3 family|</ins>IS''3''<ins class="diffchange diffchange-inline">]] </ins>itself where strong stimulation of transposition has been observed in a dam-host, in most of these cases the biological relevance of these sites is unknown. Moreover, it should be pointed out that the probability that any 100 bp DNA sequence carries the GATC tetranucleotide is about 40%. The role of Dam methylation in IS''10'' and IS''50'' transposition is described in detail in the appropriate sections dealing with these elements.</div></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>====Metabolic control elements====</div></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>====Metabolic control elements====</div></td></tr>
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<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>====Hfq====</div></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>====Hfq====</div></td></tr>
<tr><td class='diff-marker'>−</td><td style="color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div>Finally, the RNA chaperone Hfq has also been implicated in the regulation of Tn''10'' transposition by promoting RNAout interaction with transposase mRNA<ref><nowiki><pubmed>23510801</pubmed></nowiki></ref><ref><nowiki><pubmed>25649688</pubmed></nowiki></ref><ref><nowiki><pubmed>25579599</pubmed></nowiki></ref>.</div></td><td class='diff-marker'>+</td><td style="color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div>Finally, the RNA chaperone <ins class="diffchange diffchange-inline">[[wikipedia:Hfq_protein|</ins>Hfq<ins class="diffchange diffchange-inline">]] </ins>has also been implicated in the regulation of Tn''10'' transposition by promoting RNAout interaction with transposase mRNA<ref><nowiki><pubmed>23510801</pubmed></nowiki></ref><ref><nowiki><pubmed>25649688</pubmed></nowiki></ref><ref><nowiki><pubmed>25579599</pubmed></nowiki></ref>.</div></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>===Over-production inhibition===</div></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>===Over-production inhibition===</div></td></tr>
</table>TnCentralhttps://tncentral.ncc.unesp.br/TnPedia/index.php?title=General_Information/ClpX,_ClpP,_and_Lon&diff=1104&oldid=prevTnCentral at 18:53, 3 June 20202020-06-03T18:53:21Z<p></p>
<table class="diff diff-contentalign-left" data-mw="interface">
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<td colspan="2" style="background-color: #fff; color: #222; text-align: center;">← Older revision</td>
<td colspan="2" style="background-color: #fff; color: #222; text-align: center;">Revision as of 18:53, 3 June 2020</td>
</tr><tr><td colspan="2" class="diff-lineno" id="mw-diff-left-l1" >Line 1:</td>
<td colspan="2" class="diff-lineno">Line 1:</td></tr>
<tr><td colspan="2"> </td><td class='diff-marker'>+</td><td style="color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">====General====</ins></div></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>'''<big>C</big>'''ertain factors involved in protein "management" such as ClpX, ClpP, and Lon have been implicated in transposition. ClpX is essential for Mu growth<ref><nowiki><pubmed>8022280</pubmed></nowiki></ref> where it is required for disassembling the transposase-DNA complex or the transpososome strand transfer complex in preparation for the assembly of a replication complex<ref><nowiki><pubmed>8631314</pubmed></nowiki></ref><ref><nowiki><pubmed>7557391</pubmed></nowiki></ref>. Recognition of Mu transposase, pA, by ClpX requires the terminal 10 amino acids of pA<ref><nowiki><pubmed>9203582</pubmed></nowiki></ref>. Together with ClpP, ClpX also plays a role in proteolysis of the Mu repressor<ref><nowiki><pubmed>8617219</pubmed></nowiki></ref><ref><nowiki><pubmed>9299335</pubmed></nowiki></ref>. The Lon protease is implicated in proteolysis of the IS''903'' transposase<ref><nowiki><pubmed>2161528</pubmed></nowiki></ref>.</div></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>'''<big>C</big>'''ertain factors involved in protein "management" such as ClpX, ClpP, and Lon have been implicated in transposition. ClpX is essential for Mu growth<ref><nowiki><pubmed>8022280</pubmed></nowiki></ref> where it is required for disassembling the transposase-DNA complex or the transpososome strand transfer complex in preparation for the assembly of a replication complex<ref><nowiki><pubmed>8631314</pubmed></nowiki></ref><ref><nowiki><pubmed>7557391</pubmed></nowiki></ref>. Recognition of Mu transposase, pA, by ClpX requires the terminal 10 amino acids of pA<ref><nowiki><pubmed>9203582</pubmed></nowiki></ref>. Together with ClpP, ClpX also plays a role in proteolysis of the Mu repressor<ref><nowiki><pubmed>8617219</pubmed></nowiki></ref><ref><nowiki><pubmed>9299335</pubmed></nowiki></ref>. The Lon protease is implicated in proteolysis of the IS''903'' transposase<ref><nowiki><pubmed>2161528</pubmed></nowiki></ref>.</div></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"></td></tr>
</table>TnCentralhttps://tncentral.ncc.unesp.br/TnPedia/index.php?title=General_Information/ClpX,_ClpP,_and_Lon&diff=1103&oldid=prevTnCentral at 18:53, 3 June 20202020-06-03T18:53:01Z<p></p>
<table class="diff diff-contentalign-left" data-mw="interface">
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<td colspan="2" style="background-color: #fff; color: #222; text-align: center;">← Older revision</td>
<td colspan="2" style="background-color: #fff; color: #222; text-align: center;">Revision as of 18:53, 3 June 2020</td>
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<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>====SOS system, RecA, RecBC====</div></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>====SOS system, RecA, RecBC====</div></td></tr>
<tr><td class='diff-marker'>−</td><td style="color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div>The third class of host factor includes host cell systems which act to limit DNA damage and maintain chromosome integrity. Studies with IS''10'' (see <ref><nowiki><pubmed>8556869</pubmed></nowiki></ref> and IS''1''<ref><nowiki><pubmed>7932694</pubmed></nowiki></ref> have demonstrated that high levels of Tpase in the presence of suitable terminal IRs lead to induction of the host [[wikipedia:SOS_response|SOS system]]. As discussed previously<ref><nowiki><pubmed>9729608</pubmed></nowiki></ref>, some controversy still exists concerning the role of RecA in Tn''5'' (IS''50'') transposition<ref><nowiki><pubmed>1648004</pubmed></nowiki></ref><ref><nowiki><pubmed>1655708</pubmed></nowiki></ref><ref><nowiki><pubmed>1657870</pubmed></nowiki></ref>. Reznikoff and colleagues have provided genetic evidence that transposition is inhibited by induction of the SOS system in a manner which does not require the proteolytic activity of RecA<ref><nowiki><pubmed>1657870</pubmed></nowiki></ref>. On the other hand, Tessman and collaborators<ref><nowiki><pubmed>1648004</pubmed></nowiki></ref><ref><nowiki><pubmed>1655708</pubmed></nowiki></ref><ref><nowiki><pubmed>1328165</pubmed></nowiki></ref> using a different transposition assay have found that constitutive SOS conditions actually enhance Tn''5'' transposition. Moreover, using yet another assay system, Ahmed<ref><nowiki><pubmed>3025455</pubmed></nowiki></ref> has concluded that intermolecular transposition of Tn''5'' is stimulated by RecA. Further investigation is clearly required to understand these apparently incompatible results.</div></td><td class='diff-marker'>+</td><td style="color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div>The third class of host factor includes host cell systems which act to limit DNA damage and maintain chromosome integrity. Studies with IS''10'' (see <ref><nowiki><pubmed>8556869</pubmed></nowiki></ref><ins class="diffchange diffchange-inline">) </ins>and IS''1''<ref><nowiki><pubmed>7932694</pubmed></nowiki></ref> have demonstrated that high levels of Tpase in the presence of suitable terminal IRs lead to induction of the host [[wikipedia:SOS_response|SOS system]]. As discussed previously<ref><nowiki><pubmed>9729608</pubmed></nowiki></ref>, some controversy still exists concerning the role of RecA in Tn''5'' (IS''50'') transposition<ref><nowiki><pubmed>1648004</pubmed></nowiki></ref><ref><nowiki><pubmed>1655708</pubmed></nowiki></ref><ref><nowiki><pubmed>1657870</pubmed></nowiki></ref>. Reznikoff and colleagues have provided genetic evidence that transposition is inhibited by induction of the SOS system in a manner which does not require the proteolytic activity of RecA<ref><nowiki><pubmed>1657870</pubmed></nowiki></ref>. On the other hand, Tessman and collaborators<ref><nowiki><pubmed>1648004</pubmed></nowiki></ref><ref><nowiki><pubmed>1655708</pubmed></nowiki></ref><ref><nowiki><pubmed>1328165</pubmed></nowiki></ref> using a different transposition assay have found that constitutive SOS conditions actually enhance Tn''5'' transposition. Moreover, using yet another assay system, Ahmed<ref><nowiki><pubmed>3025455</pubmed></nowiki></ref> has concluded that intermolecular transposition of Tn''5'' is stimulated by RecA. Further investigation is clearly required to understand these apparently incompatible results.</div></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>Ahmed has also concluded that intermolecular transposition of the IS''1''-based transposon, Tn''9'', behaves in a similar way to that of Tn''5'' with respect to the recA allele<ref><nowiki><pubmed>3025455</pubmed></nowiki></ref>. In contrast, however, the frequency of adjacent deletions mediated by IS''1'' was significantly increased in the absence of RecA. This has received some independent support using a physical assay where it was shown that deletion products accumulate in a recA but not in a wildtype host. Moreover, like IS''1'' induction of the [[wikipedia:SOS_response|SOS system]], accumulation of such adjacent deletions was dependent on ''recBC'' (Zablweska et al., unpublished observations). The ''recBC'' genes are also implicated in the behavior of transposons such as Tn''10'' and Tn''5''<ref><nowiki><pubmed>3025455</pubmed></nowiki></ref><ref><nowiki><pubmed>6322169</pubmed></nowiki></ref> where they affect precise and imprecise excision in a process independent of transposition per se. This is more pronounced with composite transposons in which the component insertion sequences IS''10'' and IS''50'' are present as inverted repeats, and is stimulated when the transposon is carried by a transfer-proficient conjugative plasmid. It seems probable that such excisions occur by a process involving replication fork slippage (see <ref><nowiki><pubmed>10844241</pubmed></nowiki></ref><ref><nowiki><pubmed>10715006</pubmed></nowiki></ref> for further discussion).</div></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>Ahmed has also concluded that intermolecular transposition of the IS''1''-based transposon, Tn''9'', behaves in a similar way to that of Tn''5'' with respect to the recA allele<ref><nowiki><pubmed>3025455</pubmed></nowiki></ref>. In contrast, however, the frequency of adjacent deletions mediated by IS''1'' was significantly increased in the absence of RecA. This has received some independent support using a physical assay where it was shown that deletion products accumulate in a recA but not in a wildtype host. Moreover, like IS''1'' induction of the [[wikipedia:SOS_response|SOS system]], accumulation of such adjacent deletions was dependent on ''recBC'' (Zablweska et al., unpublished observations). The ''recBC'' genes are also implicated in the behavior of transposons such as Tn''10'' and Tn''5''<ref><nowiki><pubmed>3025455</pubmed></nowiki></ref><ref><nowiki><pubmed>6322169</pubmed></nowiki></ref> where they affect precise and imprecise excision in a process independent of transposition per se. This is more pronounced with composite transposons in which the component insertion sequences IS''10'' and IS''50'' are present as inverted repeats, and is stimulated when the transposon is carried by a transfer-proficient conjugative plasmid. It seems probable that such excisions occur by a process involving replication fork slippage (see <ref><nowiki><pubmed>10844241</pubmed></nowiki></ref><ref><nowiki><pubmed>10715006</pubmed></nowiki></ref> for further discussion).</div></td></tr>
</table>TnCentralhttps://tncentral.ncc.unesp.br/TnPedia/index.php?title=General_Information/ClpX,_ClpP,_and_Lon&diff=815&oldid=prevTnCentral at 22:01, 21 May 20202020-05-21T22:01:01Z<p></p>
<table class="diff diff-contentalign-left" data-mw="interface">
<col class="diff-marker" />
<col class="diff-content" />
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<tr class="diff-title" lang="en">
<td colspan="2" style="background-color: #fff; color: #222; text-align: center;">← Older revision</td>
<td colspan="2" style="background-color: #fff; color: #222; text-align: center;">Revision as of 22:01, 21 May 2020</td>
</tr><tr><td colspan="2" class="diff-lineno" id="mw-diff-left-l1" >Line 1:</td>
<td colspan="2" class="diff-lineno">Line 1:</td></tr>
<tr><td class='diff-marker'>−</td><td style="color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div>'''<big>C</big>'''ertain factors involved in protein "management" such as ClpX, ClpP, and Lon have been implicated in transposition. ClpX is essential for Mu growth<ref><nowiki><pubmed>8022280</pubmed></nowiki></ref> where it is required for disassembling the transposase-DNA complex or the transpososome strand transfer complex in preparation for the assembly of a replication complex<ref><nowiki><pubmed>8631314</pubmed></nowiki></ref><ref><nowiki><pubmed>7557391</pubmed></nowiki></ref>. Recognition of Mu transposase, pA, by ClpX requires the terminal 10 amino acids of pA<ref><nowiki><pubmed>9203582</pubmed></nowiki></ref>. Together with ClpP, ClpX also plays a role in proteolysis of the Mu repressor<ref><nowiki><pubmed>8617219</pubmed></nowiki></ref><ref><nowiki><pubmed>9299335</pubmed></nowiki></ref>. The Lon protease is implicated in proteolysis of the <del class="diffchange diffchange-inline">IS903 </del>transposase<ref><nowiki><pubmed>2161528</pubmed></nowiki></ref>.</div></td><td class='diff-marker'>+</td><td style="color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div>'''<big>C</big>'''ertain factors involved in protein "management" such as ClpX, ClpP, and Lon have been implicated in transposition. ClpX is essential for Mu growth<ref><nowiki><pubmed>8022280</pubmed></nowiki></ref> where it is required for disassembling the transposase-DNA complex or the transpososome strand transfer complex in preparation for the assembly of a replication complex<ref><nowiki><pubmed>8631314</pubmed></nowiki></ref><ref><nowiki><pubmed>7557391</pubmed></nowiki></ref>. Recognition of Mu transposase, pA, by ClpX requires the terminal 10 amino acids of pA<ref><nowiki><pubmed>9203582</pubmed></nowiki></ref>. Together with ClpP, ClpX also plays a role in proteolysis of the Mu repressor<ref><nowiki><pubmed>8617219</pubmed></nowiki></ref><ref><nowiki><pubmed>9299335</pubmed></nowiki></ref>. The Lon protease is implicated in proteolysis of the <ins class="diffchange diffchange-inline">IS''903'' </ins>transposase<ref><nowiki><pubmed>2161528</pubmed></nowiki></ref>.</div></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>At present the involvement of these proteins in the transposition of other elements has not been well documented.</div></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>At present the involvement of these proteins in the transposition of other elements has not been well documented.</div></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>====SOS system, RecA, RecBC====</div></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>====SOS system, RecA, RecBC====</div></td></tr>
<tr><td class='diff-marker'>−</td><td style="color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div>The third class of host factor includes host cell systems which act to limit DNA damage and maintain chromosome integrity. Studies with IS''10'' (see <ref><nowiki><pubmed>8556869</pubmed></nowiki></ref> and IS''1''<ref><nowiki><pubmed>7932694</pubmed></nowiki></ref> have demonstrated that high levels of Tpase in the presence of suitable terminal IRs lead to induction of the host SOS system. As discussed previously<ref><nowiki><pubmed>9729608</pubmed></nowiki></ref>, some controversy still exists concerning the role of RecA in Tn''5'' (IS''50'') transposition<ref><nowiki><pubmed>1648004</pubmed></nowiki></ref><ref><nowiki><pubmed>1655708</pubmed></nowiki></ref><ref><nowiki><pubmed>1657870</pubmed></nowiki></ref>. Reznikoff and colleagues have provided genetic evidence that transposition is inhibited by induction of the SOS system in a manner which does not require the proteolytic activity of RecA<ref><nowiki><pubmed>1657870</pubmed></nowiki></ref>. On the other hand, Tessman and collaborators<ref><nowiki><pubmed>1648004</pubmed></nowiki></ref><ref><nowiki><pubmed>1655708</pubmed></nowiki></ref><ref><nowiki><pubmed>1328165</pubmed></nowiki></ref> using a different transposition assay have found that constitutive SOS conditions actually enhance Tn''5'' transposition. Moreover, using yet another assay system, Ahmed<ref><nowiki><pubmed>3025455</pubmed></nowiki></ref> has concluded that intermolecular transposition of Tn''5'' is stimulated by RecA. Further investigation is clearly required to understand these apparently incompatible results.</div></td><td class='diff-marker'>+</td><td style="color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div>The third class of host factor includes host cell systems which act to limit DNA damage and maintain chromosome integrity. Studies with IS''10'' (see <ref><nowiki><pubmed>8556869</pubmed></nowiki></ref> and IS''1''<ref><nowiki><pubmed>7932694</pubmed></nowiki></ref> have demonstrated that high levels of Tpase in the presence of suitable terminal IRs lead to induction of the host <ins class="diffchange diffchange-inline">[[wikipedia:SOS_response|</ins>SOS system<ins class="diffchange diffchange-inline">]]</ins>. As discussed previously<ref><nowiki><pubmed>9729608</pubmed></nowiki></ref>, some controversy still exists concerning the role of RecA in Tn''5'' (IS''50'') transposition<ref><nowiki><pubmed>1648004</pubmed></nowiki></ref><ref><nowiki><pubmed>1655708</pubmed></nowiki></ref><ref><nowiki><pubmed>1657870</pubmed></nowiki></ref>. Reznikoff and colleagues have provided genetic evidence that transposition is inhibited by induction of the SOS system in a manner which does not require the proteolytic activity of RecA<ref><nowiki><pubmed>1657870</pubmed></nowiki></ref>. On the other hand, Tessman and collaborators<ref><nowiki><pubmed>1648004</pubmed></nowiki></ref><ref><nowiki><pubmed>1655708</pubmed></nowiki></ref><ref><nowiki><pubmed>1328165</pubmed></nowiki></ref> using a different transposition assay have found that constitutive SOS conditions actually enhance Tn''5'' transposition. Moreover, using yet another assay system, Ahmed<ref><nowiki><pubmed>3025455</pubmed></nowiki></ref> has concluded that intermolecular transposition of Tn''5'' is stimulated by RecA. Further investigation is clearly required to understand these apparently incompatible results.</div></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"></td></tr>
<tr><td class='diff-marker'>−</td><td style="color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div>Ahmed has also concluded that intermolecular transposition of the IS''1''-based transposon, Tn''9'', behaves in a similar way to that of Tn''5'' with respect to the recA allele<ref><nowiki><pubmed>3025455</pubmed></nowiki></ref>. In contrast, however, the frequency of adjacent deletions mediated by IS''1'' was significantly increased in the absence of RecA. This has received some independent support using a physical assay where it was shown that deletion products accumulate in a recA but not in a wildtype host. Moreover, like IS''1'' induction of the SOS system, accumulation of such adjacent deletions was dependent on ''recBC'' (Zablweska et al., unpublished observations). The ''recBC'' genes are also implicated in the behavior of transposons such as Tn''10'' and Tn''5''<ref><nowiki><pubmed>3025455</pubmed></nowiki></ref><ref><nowiki><pubmed>6322169</pubmed></nowiki></ref> where they affect precise and imprecise excision in a process independent of transposition per se. This is more pronounced with composite transposons in which the component insertion sequences IS''10'' and IS''50'' are present as inverted repeats, and is stimulated when the transposon is carried by a transfer-proficient conjugative plasmid. It seems probable that such excisions occur by a process involving replication fork slippage (see <ref><nowiki><pubmed>10844241</pubmed></nowiki></ref><ref><nowiki><pubmed>10715006</pubmed></nowiki></ref> for further discussion).</div></td><td class='diff-marker'>+</td><td style="color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div>Ahmed has also concluded that intermolecular transposition of the IS''1''-based transposon, Tn''9'', behaves in a similar way to that of Tn''5'' with respect to the recA allele<ref><nowiki><pubmed>3025455</pubmed></nowiki></ref>. In contrast, however, the frequency of adjacent deletions mediated by IS''1'' was significantly increased in the absence of RecA. This has received some independent support using a physical assay where it was shown that deletion products accumulate in a recA but not in a wildtype host. Moreover, like IS''1'' induction of the <ins class="diffchange diffchange-inline">[[wikipedia:SOS_response|</ins>SOS system<ins class="diffchange diffchange-inline">]]</ins>, accumulation of such adjacent deletions was dependent on ''recBC'' (Zablweska et al., unpublished observations). The ''recBC'' genes are also implicated in the behavior of transposons such as Tn''10'' and Tn''5''<ref><nowiki><pubmed>3025455</pubmed></nowiki></ref><ref><nowiki><pubmed>6322169</pubmed></nowiki></ref> where they affect precise and imprecise excision in a process independent of transposition per se. This is more pronounced with composite transposons in which the component insertion sequences IS''10'' and IS''50'' are present as inverted repeats, and is stimulated when the transposon is carried by a transfer-proficient conjugative plasmid. It seems probable that such excisions occur by a process involving replication fork slippage (see <ref><nowiki><pubmed>10844241</pubmed></nowiki></ref><ref><nowiki><pubmed>10715006</pubmed></nowiki></ref> for further discussion).</div></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>====PolI and gyrase====</div></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>====PolI and gyrase====</div></td></tr>
<tr><td colspan="2" class="diff-lineno" id="mw-diff-left-l15" >Line 15:</td>
<td colspan="2" class="diff-lineno">Line 15:</td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>====Metabolic control elements====</div></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>====Metabolic control elements====</div></td></tr>
<tr><td class='diff-marker'>−</td><td style="color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div>In a screen of over 20,000 independent insertion mutants for host factors that influence IS''903'' transposition the Derbyshire lab isolated more than 100 mutants that increased or decreased transposition and also altered its timing during colony growth<ref><nowiki><pubmed>16135227</pubmed></nowiki></ref>. These included independent mutations in a gene required for fermentative metabolism during anaerobic growth resulting in “early” transposition during colony growth and was suppressed by addition of fumarate, and other mutations in genes associated with DNA metabolism, intermediary metabolism, transport, cellular redox, protein folding and proteolysis. Other mutations were isolated in pur genes involved in purine biosynthesis. Further analysis suggested that this phenotype was due to a requirement for GTP in IS''903'' transposition<ref><nowiki><pubmed>15968071</pubmed></nowiki></ref>. It should be noted that some of these mutants also affected transposition of IS''10'' and of Tn''552''.</div></td><td class='diff-marker'>+</td><td style="color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div>In a screen of over 20,000 independent insertion mutants for host factors that influence IS''903'' transposition the <ins class="diffchange diffchange-inline">[https://www.derbylab.org/ </ins>Derbyshire lab<ins class="diffchange diffchange-inline">] </ins>isolated more than 100 mutants that increased or decreased transposition and also altered its timing during colony growth<ref><nowiki><pubmed>16135227</pubmed></nowiki></ref>. These included independent mutations in a gene required for fermentative metabolism during anaerobic growth resulting in “early” transposition during colony growth and was suppressed by addition of fumarate, and other mutations in genes associated with DNA metabolism, intermediary metabolism, transport, cellular redox, protein folding and proteolysis. Other mutations were isolated in pur genes involved in purine biosynthesis. Further analysis suggested that this phenotype was due to a requirement for GTP in IS''903'' transposition<ref><nowiki><pubmed>15968071</pubmed></nowiki></ref>. It should be noted that some of these mutants also affected transposition of IS''10'' and of Tn''552''.</div></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>====Hfq====</div></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>====Hfq====</div></td></tr>
</table>TnCentralhttps://tncentral.ncc.unesp.br/TnPedia/index.php?title=General_Information/ClpX,_ClpP,_and_Lon&diff=793&oldid=prevTnCentral at 18:00, 21 May 20202020-05-21T18:00:45Z<p></p>
<table class="diff diff-contentalign-left" data-mw="interface">
<col class="diff-marker" />
<col class="diff-content" />
<col class="diff-marker" />
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<td colspan="2" style="background-color: #fff; color: #222; text-align: center;">← Older revision</td>
<td colspan="2" style="background-color: #fff; color: #222; text-align: center;">Revision as of 18:00, 21 May 2020</td>
</tr><tr><td colspan="2" class="diff-lineno" id="mw-diff-left-l25" >Line 25:</td>
<td colspan="2" class="diff-lineno">Line 25:</td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>The biological rational for this is that “infection” of a naïve cell by the transposon results in a burst of transposition which is then attenuated by overproduction inhibition. This is then followed by gradual decay of the transposon.</div></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>The biological rational for this is that “infection” of a naïve cell by the transposon results in a burst of transposition which is then attenuated by overproduction inhibition. This is then followed by gradual decay of the transposon.</div></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"></td></tr>
<tr><td class='diff-marker'>−</td><td style="color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div>The Chalmers lab<ref><nowiki><pubmed>23795293</pubmed></nowiki></ref> has provided an interesting and compelling explanation of this effect. Using the mariner family transposon Hsmar1 they present convincing data implying that overproduction inhibition occurs during transpososome assembly and is due to a combination of the multimeric state of the transposase coupled with competition for transposase binding sites at the Hsmar1 ends<ref><nowiki><pubmed>24812590</pubmed></nowiki></ref><ref><nowiki><pubmed>26104691</pubmed></nowiki></ref>. The model (assembly-site-occlusion model) is based on the presence of transposase multimers (dimers) to the exclusion of monomers – in other words, end-binding required a dimeric transposase. At low transposase/transposon ratios, one dimer can bind both transposon ends resulting in the ordered assembly of the transpososome. An increase in the transposase dimer/transposon ratio results in binding of dimers to both transposon ends, preventing transpososome assembly. The model not only explains the ''in vivo'' transposase dose-response for Hsmar1 but also for the related Sleeping Beauty (SB) and piggyBac (PB) transposons. As yet, no information is at present available concerning the relevance of this mode of regulation to prokaryotic transposable elements.</div></td><td class='diff-marker'>+</td><td style="color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div>The <ins class="diffchange diffchange-inline">[https://chalmerslab.wordpress.com/research/ </ins>Chalmers lab<ins class="diffchange diffchange-inline">]</ins><ref><nowiki><pubmed>23795293</pubmed></nowiki></ref> has provided an interesting and compelling explanation of this effect. Using the mariner family transposon Hsmar1 they present convincing data implying that overproduction inhibition occurs during transpososome assembly and is due to a combination of the multimeric state of the transposase coupled with competition for transposase binding sites at the Hsmar1 ends<ref><nowiki><pubmed>24812590</pubmed></nowiki></ref><ref><nowiki><pubmed>26104691</pubmed></nowiki></ref>. The model (assembly-site-occlusion model) is based on the presence of transposase multimers (dimers) to the exclusion of monomers – in other words, end-binding required a dimeric transposase. At low transposase/transposon ratios, one dimer can bind both transposon ends resulting in the ordered assembly of the transpososome. An increase in the transposase dimer/transposon ratio results in binding of dimers to both transposon ends, preventing transpososome assembly. The model not only explains the ''in vivo'' transposase dose-response for Hsmar1 but also for the related Sleeping Beauty (SB) and piggyBac (PB) transposons. As yet, no information is at present available concerning the relevance of this mode of regulation to prokaryotic transposable elements.</div></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>==Bibliography==</div></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>==Bibliography==</div></td></tr>
</table>TnCentralhttps://tncentral.ncc.unesp.br/TnPedia/index.php?title=General_Information/ClpX,_ClpP,_and_Lon&diff=637&oldid=prevTnCentral at 19:48, 5 May 20202020-05-05T19:48:22Z<p></p>
<table class="diff diff-contentalign-left" data-mw="interface">
<col class="diff-marker" />
<col class="diff-content" />
<col class="diff-marker" />
<col class="diff-content" />
<tr class="diff-title" lang="en">
<td colspan="2" style="background-color: #fff; color: #222; text-align: center;">← Older revision</td>
<td colspan="2" style="background-color: #fff; color: #222; text-align: center;">Revision as of 19:48, 5 May 2020</td>
</tr><tr><td colspan="2" class="diff-lineno" id="mw-diff-left-l4" >Line 4:</td>
<td colspan="2" class="diff-lineno">Line 4:</td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>====SOS system, RecA, RecBC====</div></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>====SOS system, RecA, RecBC====</div></td></tr>
<tr><td class='diff-marker'>−</td><td style="color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div>The third class of host factor includes host cell systems which act to limit DNA damage and maintain chromosome integrity. Studies with IS''10'' (see <ref><nowiki><pubmed>8556869</pubmed></nowiki></ref> and IS''1''<ref><nowiki><pubmed>7932694</pubmed></nowiki></ref> have demonstrated that high levels of Tpase in the presence of suitable terminal IRs lead to induction of the host SOS system. As discussed previously<ref><nowiki><pubmed>9729608</pubmed></nowiki></ref>, some controversy still exists concerning the role of RecA in Tn''5'' (IS''50'') transposition<ref><nowiki><pubmed>1648004</pubmed></nowiki></ref><ref><nowiki><pubmed>1655708</pubmed></nowiki></ref><ref><nowiki><pubmed>1657870</pubmed></nowiki></ref>. Reznikoff and colleagues have provided genetic evidence that transposition is inhibited by induction of the SOS system in a manner which does not require the proteolytic activity of RecA<ref><nowiki><pubmed>1657870</pubmed></nowiki></ref>. On the other hand, Tessman and collaborators<ref><nowiki><pubmed>1648004</pubmed></nowiki></ref><ref><nowiki><pubmed>1655708</pubmed></nowiki></ref><ref><nowiki><pubmed>1328165</pubmed></nowiki></ref> using a different transposition assay have found that constitutive SOS conditions actually enhance <del class="diffchange diffchange-inline">Tn5 </del>transposition. Moreover, using yet another assay system, Ahmed<ref><nowiki><pubmed>3025455</pubmed></nowiki></ref> has concluded that intermolecular transposition of <del class="diffchange diffchange-inline">Tn5 </del>is stimulated by RecA. Further investigation is clearly required to understand these apparently incompatible results.</div></td><td class='diff-marker'>+</td><td style="color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div>The third class of host factor includes host cell systems which act to limit DNA damage and maintain chromosome integrity. Studies with IS''10'' (see <ref><nowiki><pubmed>8556869</pubmed></nowiki></ref> and IS''1''<ref><nowiki><pubmed>7932694</pubmed></nowiki></ref> have demonstrated that high levels of Tpase in the presence of suitable terminal IRs lead to induction of the host SOS system. As discussed previously<ref><nowiki><pubmed>9729608</pubmed></nowiki></ref>, some controversy still exists concerning the role of RecA in Tn''5'' (IS''50'') transposition<ref><nowiki><pubmed>1648004</pubmed></nowiki></ref><ref><nowiki><pubmed>1655708</pubmed></nowiki></ref><ref><nowiki><pubmed>1657870</pubmed></nowiki></ref>. Reznikoff and colleagues have provided genetic evidence that transposition is inhibited by induction of the SOS system in a manner which does not require the proteolytic activity of RecA<ref><nowiki><pubmed>1657870</pubmed></nowiki></ref>. On the other hand, Tessman and collaborators<ref><nowiki><pubmed>1648004</pubmed></nowiki></ref><ref><nowiki><pubmed>1655708</pubmed></nowiki></ref><ref><nowiki><pubmed>1328165</pubmed></nowiki></ref> using a different transposition assay have found that constitutive SOS conditions actually enhance <ins class="diffchange diffchange-inline">Tn''5'' </ins>transposition. Moreover, using yet another assay system, Ahmed<ref><nowiki><pubmed>3025455</pubmed></nowiki></ref> has concluded that intermolecular transposition of <ins class="diffchange diffchange-inline">Tn''5'' </ins>is stimulated by RecA. Further investigation is clearly required to understand these apparently incompatible results.</div></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"></td></tr>
<tr><td class='diff-marker'>−</td><td style="color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div>Ahmed has also concluded that intermolecular transposition of the IS''1''-based transposon, Tn''9'', behaves in a similar way to that of Tn''5'' with respect to the recA allele<ref><nowiki><pubmed>3025455</pubmed></nowiki></ref>. In contrast, however, the frequency of adjacent deletions mediated by IS''1'' was significantly increased in the absence of RecA. This has received some independent support using a physical assay where it was shown that deletion products accumulate in a recA but not in a wildtype host. Moreover, like IS''1'' induction of the SOS system, accumulation of such adjacent deletions was dependent on recBC (Zablweska et al., unpublished observations). The recBC genes are also implicated in the behavior of transposons such as Tn''10'' and Tn''5''<ref><nowiki><pubmed>3025455</pubmed></nowiki></ref><ref><nowiki><pubmed>6322169</pubmed></nowiki></ref> where they affect precise and imprecise excision in a process independent of transposition per se. This is more pronounced with composite transposons in which the component insertion sequences IS''10'' and IS''50'' are present as inverted repeats, and is stimulated when the transposon is carried by a transfer-proficient conjugative plasmid. It seems probable that such excisions occur by a process involving replication fork slippage (see <ref><nowiki><pubmed>10844241</pubmed></nowiki></ref><ref><nowiki><pubmed>10715006</pubmed></nowiki></ref> for further discussion).</div></td><td class='diff-marker'>+</td><td style="color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div>Ahmed has also concluded that intermolecular transposition of the IS''1''-based transposon, Tn''9'', behaves in a similar way to that of Tn''5'' with respect to the recA allele<ref><nowiki><pubmed>3025455</pubmed></nowiki></ref>. In contrast, however, the frequency of adjacent deletions mediated by IS''1'' was significantly increased in the absence of RecA. This has received some independent support using a physical assay where it was shown that deletion products accumulate in a recA but not in a wildtype host. Moreover, like IS''1'' induction of the SOS system, accumulation of such adjacent deletions was dependent on <ins class="diffchange diffchange-inline">''</ins>recBC<ins class="diffchange diffchange-inline">'' </ins>(Zablweska et al., unpublished observations). The <ins class="diffchange diffchange-inline">''</ins>recBC<ins class="diffchange diffchange-inline">'' </ins>genes are also implicated in the behavior of transposons such as Tn''10'' and Tn''5''<ref><nowiki><pubmed>3025455</pubmed></nowiki></ref><ref><nowiki><pubmed>6322169</pubmed></nowiki></ref> where they affect precise and imprecise excision in a process independent of transposition per se. This is more pronounced with composite transposons in which the component insertion sequences IS''10'' and IS''50'' are present as inverted repeats, and is stimulated when the transposon is carried by a transfer-proficient conjugative plasmid. It seems probable that such excisions occur by a process involving replication fork slippage (see <ref><nowiki><pubmed>10844241</pubmed></nowiki></ref><ref><nowiki><pubmed>10715006</pubmed></nowiki></ref> for further discussion).</div></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>====PolI and gyrase====</div></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>====PolI and gyrase====</div></td></tr>
<tr><td class='diff-marker'>−</td><td style="color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div>Both DNA polymerase I<ref><nowiki><pubmed>6267432</pubmed></nowiki></ref><ref><nowiki><pubmed>6288966</pubmed></nowiki></ref><ref><nowiki><pubmed>3030303</pubmed></nowiki></ref> and DNA gyrase<ref><nowiki><pubmed>6290084</pubmed></nowiki></ref><ref><nowiki><pubmed>6265907</pubmed></nowiki></ref> are implicated in the transposition of Tn''5''. While the effect of gyrase may reflect a requirement for optimal levels of supercoiling, the role of PolI remains a matter of speculation. It may be involved in DNA synthesis necessary to repair the single strand gaps resulting from staggered cleavage of the target and which gives rise to the DRs. DNA gyrase has also been shown to be important in transposition of [[wikipedia:Bacteriophage_Mu|bacteriophage Mu]]<ref><nowiki><pubmed>7592347</pubmed></nowiki></ref><ref><nowiki><pubmed>8930913</pubmed></nowiki></ref>.</div></td><td class='diff-marker'>+</td><td style="color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div>Both DNA polymerase I <ref><nowiki><pubmed>6267432</pubmed></nowiki></ref><ref><nowiki><pubmed>6288966</pubmed></nowiki></ref><ref><nowiki><pubmed>3030303</pubmed></nowiki></ref> and DNA gyrase<ref><nowiki><pubmed>6290084</pubmed></nowiki></ref><ref><nowiki><pubmed>6265907</pubmed></nowiki></ref> are implicated in the transposition of Tn''5''. While the effect of gyrase may reflect a requirement for optimal levels of supercoiling, the role of PolI remains a matter of speculation. It may be involved in DNA synthesis necessary to repair the single strand gaps resulting from staggered cleavage of the target and which gives rise to the DRs. DNA gyrase has also been shown to be important in transposition of [[wikipedia:Bacteriophage_Mu|bacteriophage Mu]]<ref><nowiki><pubmed>7592347</pubmed></nowiki></ref><ref><nowiki><pubmed>8930913</pubmed></nowiki></ref>.</div></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>====Dam methylase====</div></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>====Dam methylase====</div></td></tr>
<tr><td colspan="2" class="diff-lineno" id="mw-diff-left-l21" >Line 21:</td>
<td colspan="2" class="diff-lineno">Line 21:</td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>===Over-production inhibition===</div></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>===Over-production inhibition===</div></td></tr>
<tr><td class='diff-marker'>−</td><td style="color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div>Certain transposons appear to be subject to a mode of regulation known as over-expression inhibition. This was first observed with the eukaryotic transposons Tc1/mariner Lampe<ref><nowiki><pubmed>9584095</pubmed></nowiki></ref><ref><nowiki><pubmed>8882498</pubmed></nowiki></ref><ref><nowiki><pubmed>9154003</pubmed></nowiki></ref> where increasing the concentration of transposase results in a reduction in the level of transposition. It was subsequently observed with the sleeping beauty transposon<ref><nowiki><pubmed>12842434</pubmed></nowiki></ref><ref><nowiki><pubmed>14759813</pubmed></nowiki></ref>. It also occurs in vivo in mice<ref><nowiki><pubmed>14961361</pubmed></nowiki></ref><ref><nowiki><pubmed>14529839</pubmed></nowiki></ref>.</div></td><td class='diff-marker'>+</td><td style="color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div>Certain transposons appear to be subject to a mode of regulation known as over-expression inhibition. This was first observed with the eukaryotic transposons Tc1/mariner Lampe<ref><nowiki><pubmed>9584095</pubmed></nowiki></ref><ref><nowiki><pubmed>8882498</pubmed></nowiki></ref><ref><nowiki><pubmed>9154003</pubmed></nowiki></ref> where increasing the concentration of transposase results in a reduction in the level of transposition. It was subsequently observed with the sleeping beauty transposon<ref><nowiki><pubmed>12842434</pubmed></nowiki></ref><ref><nowiki><pubmed>14759813</pubmed></nowiki></ref>. It also occurs <ins class="diffchange diffchange-inline">''</ins>in vivo<ins class="diffchange diffchange-inline">'' </ins>in mice<ref><nowiki><pubmed>14961361</pubmed></nowiki></ref><ref><nowiki><pubmed>14529839</pubmed></nowiki></ref>.</div></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>The biological rational for this is that “infection” of a naïve cell by the transposon results in a burst of transposition which is then attenuated by overproduction inhibition. This is then followed by gradual decay of the transposon.</div></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>The biological rational for this is that “infection” of a naïve cell by the transposon results in a burst of transposition which is then attenuated by overproduction inhibition. This is then followed by gradual decay of the transposon.</div></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"></td></tr>
<tr><td class='diff-marker'>−</td><td style="color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div>The Chalmers lab<ref><nowiki><pubmed>23795293</pubmed></nowiki></ref> has provided an interesting and compelling explanation of this effect. Using the mariner family transposon Hsmar1 they present convincing data implying that overproduction inhibition occurs during transpososome assembly and is due to a combination of the multimeric state of the transposase coupled with competition for transposase binding sites at the Hsmar1 ends<ref><nowiki><pubmed>24812590</pubmed></nowiki></ref><ref><nowiki><pubmed>26104691</pubmed></nowiki></ref>. The model (assembly-site-occlusion model) is based on the presence of transposase multimers (dimers) to the exclusion of monomers – in other words, end-binding required a dimeric transposase. At low transposase/transposon ratios, one dimer can bind both transposon ends resulting in the ordered assembly of the transpososome. An increase in the transposase dimer/transposon ratio results in binding of dimers to both transposon ends, preventing transpososome assembly. The model not only explains the in vivo transposase dose-response for Hsmar1 but also for the related Sleeping Beauty (SB) and piggyBac (PB) transposons. As yet, no information is at present available concerning the relevance of this mode of regulation to prokaryotic transposable elements.</div></td><td class='diff-marker'>+</td><td style="color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div>The Chalmers lab<ref><nowiki><pubmed>23795293</pubmed></nowiki></ref> has provided an interesting and compelling explanation of this effect. Using the mariner family transposon Hsmar1 they present convincing data implying that overproduction inhibition occurs during transpososome assembly and is due to a combination of the multimeric state of the transposase coupled with competition for transposase binding sites at the Hsmar1 ends<ref><nowiki><pubmed>24812590</pubmed></nowiki></ref><ref><nowiki><pubmed>26104691</pubmed></nowiki></ref>. The model (assembly-site-occlusion model) is based on the presence of transposase multimers (dimers) to the exclusion of monomers – in other words, end-binding required a dimeric transposase. At low transposase/transposon ratios, one dimer can bind both transposon ends resulting in the ordered assembly of the transpososome. An increase in the transposase dimer/transposon ratio results in binding of dimers to both transposon ends, preventing transpososome assembly. The model not only explains the <ins class="diffchange diffchange-inline">''</ins>in vivo<ins class="diffchange diffchange-inline">'' </ins>transposase dose-response for Hsmar1 but also for the related Sleeping Beauty (SB) and piggyBac (PB) transposons. As yet, no information is at present available concerning the relevance of this mode of regulation to prokaryotic transposable elements.</div></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>==Bibliography==</div></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>==Bibliography==</div></td></tr>
</table>TnCentralhttps://tncentral.ncc.unesp.br/TnPedia/index.php?title=General_Information/ClpX,_ClpP,_and_Lon&diff=633&oldid=prevTnCentral at 19:36, 5 May 20202020-05-05T19:36:40Z<p></p>
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<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>====PolI and gyrase====</div></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>====PolI and gyrase====</div></td></tr>
<tr><td class='diff-marker'>−</td><td style="color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div>Both DNA polymerase I<ref><nowiki><pubmed>6267432</pubmed></nowiki></ref><ref><nowiki><pubmed>6288966</pubmed></nowiki></ref><ref><nowiki><pubmed>3030303</pubmed></nowiki></ref> and DNA gyrase<ref><nowiki><pubmed>6290084</pubmed></nowiki></ref><ref><nowiki><pubmed>6265907</pubmed></nowiki></ref> are implicated in the transposition of Tn''5''. While the effect of gyrase may reflect a requirement for optimal levels of supercoiling, the role of PolI remains a matter of speculation. It may be involved in DNA synthesis necessary to repair the single strand gaps resulting from staggered cleavage of the target and which gives rise to the DRs. DNA gyrase has also been shown to be important in transposition of bacteriophage Mu<ref><nowiki><pubmed>7592347</pubmed></nowiki></ref><ref><nowiki><pubmed>8930913</pubmed></nowiki></ref>.</div></td><td class='diff-marker'>+</td><td style="color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div>Both DNA polymerase I<ref><nowiki><pubmed>6267432</pubmed></nowiki></ref><ref><nowiki><pubmed>6288966</pubmed></nowiki></ref><ref><nowiki><pubmed>3030303</pubmed></nowiki></ref> and DNA gyrase<ref><nowiki><pubmed>6290084</pubmed></nowiki></ref><ref><nowiki><pubmed>6265907</pubmed></nowiki></ref> are implicated in the transposition of Tn''5''. While the effect of gyrase may reflect a requirement for optimal levels of supercoiling, the role of PolI remains a matter of speculation. It may be involved in DNA synthesis necessary to repair the single strand gaps resulting from staggered cleavage of the target and which gives rise to the DRs. DNA gyrase has also been shown to be important in transposition of <ins class="diffchange diffchange-inline">[[wikipedia:Bacteriophage_Mu|</ins>bacteriophage Mu<ins class="diffchange diffchange-inline">]]</ins><ref><nowiki><pubmed>7592347</pubmed></nowiki></ref><ref><nowiki><pubmed>8930913</pubmed></nowiki></ref>.</div></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>====Dam methylase====</div></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>====Dam methylase====</div></td></tr>
</table>TnCentralhttps://tncentral.ncc.unesp.br/TnPedia/index.php?title=General_Information/ClpX,_ClpP,_and_Lon&diff=535&oldid=prevTnCentral at 12:42, 4 May 20202020-05-04T12:42:15Z<p></p>
<table class="diff diff-contentalign-left" data-mw="interface">
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<col class="diff-content" />
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<td colspan="2" style="background-color: #fff; color: #222; text-align: center;">← Older revision</td>
<td colspan="2" style="background-color: #fff; color: #222; text-align: center;">Revision as of 12:42, 4 May 2020</td>
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<tr><td class='diff-marker'>−</td><td style="color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div><del class="diffchange diffchange-inline">Certain </del>factors involved in protein "management" such as ClpX, ClpP, and Lon have been implicated in transposition. ClpX is essential for Mu growth<ref><nowiki><pubmed>8022280</pubmed></nowiki></ref> where it is required for disassembling the transposase-DNA complex or the transpososome strand transfer complex in preparation for the assembly of a replication complex<ref><nowiki><pubmed>8631314</pubmed></nowiki></ref><ref><nowiki><pubmed>7557391</pubmed></nowiki></ref>. Recognition of Mu transposase, pA, by ClpX requires the terminal 10 amino acids of pA<ref><nowiki><pubmed>9203582</pubmed></nowiki></ref>. Together with ClpP, ClpX also plays a role in proteolysis of the Mu repressor<ref><nowiki><pubmed>8617219</pubmed></nowiki></ref><ref><nowiki><pubmed>9299335</pubmed></nowiki></ref>. The Lon protease is implicated in proteolysis of the IS903 transposase<ref><nowiki><pubmed>2161528</pubmed></nowiki></ref>.</div></td><td class='diff-marker'>+</td><td style="color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins class="diffchange diffchange-inline">'''<big>C</big>'''ertain </ins>factors involved in protein "management" such as ClpX, ClpP, and Lon have been implicated in transposition. ClpX is essential for Mu growth<ref><nowiki><pubmed>8022280</pubmed></nowiki></ref> where it is required for disassembling the transposase-DNA complex or the transpososome strand transfer complex in preparation for the assembly of a replication complex<ref><nowiki><pubmed>8631314</pubmed></nowiki></ref><ref><nowiki><pubmed>7557391</pubmed></nowiki></ref>. Recognition of Mu transposase, pA, by ClpX requires the terminal 10 amino acids of pA<ref><nowiki><pubmed>9203582</pubmed></nowiki></ref>. Together with ClpP, ClpX also plays a role in proteolysis of the Mu repressor<ref><nowiki><pubmed>8617219</pubmed></nowiki></ref><ref><nowiki><pubmed>9299335</pubmed></nowiki></ref>. The Lon protease is implicated in proteolysis of the IS903 transposase<ref><nowiki><pubmed>2161528</pubmed></nowiki></ref>.</div></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"></td></tr>
<tr><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>At present the involvement of these proteins in the transposition of other elements has not been well documented.</div></td><td class='diff-marker'> </td><td style="background-color: #f8f9fa; color: #222; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>At present the involvement of these proteins in the transposition of other elements has not been well documented.</div></td></tr>
</table>TnCentral