Difference between revisions of "General Information/Control of transposition activity"

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(Created page with "Transposition activity is generally maintained at a low level. An often cited reason for this is that high activities and the accompanying mutagenic effect of genome rearrange...")
 
 
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Transposition activity is generally maintained at a low level. An often cited reason for this is that high activities and the accompanying mutagenic effect of genome rearrangements would be detrimental to the host cell (see <ref><nowiki><pubmed>6320009</pubmed></nowiki></ref>). Endogenous transposase promoters, in contrast to those assembled by juxtaposition of -10 and -35 hexamers in those IS families whose transposition passes through a double-strand circular transposon intermediate, are generally weak and many are partially located in the terminal IRs. This would enable their autoregulation by Tpase binding.
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Transposition activity is generally maintained at a low level. An often-cited reason for this is that high activities and the accompanying mutagenic effect of genome rearrangements would be detrimental to the host cell (see <ref><pubmed>6320009</pubmed></ref>). Endogenous transposase promoters, in contrast to those assembled by the juxtaposition of -10 and -35 hexamers in those IS families whose transposition passes through a double-strand circular transposon intermediate, are generally weak and many are partially located in the terminal IRs. This would enable their autoregulation by Tpase binding.
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==Bibliography==
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<b>Bibliography</b>
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Latest revision as of 12:50, 5 December 2022

Transposition activity is generally maintained at a low level. An often-cited reason for this is that high activities and the accompanying mutagenic effect of genome rearrangements would be detrimental to the host cell (see [1]). Endogenous transposase promoters, in contrast to those assembled by the juxtaposition of -10 and -35 hexamers in those IS families whose transposition passes through a double-strand circular transposon intermediate, are generally weak and many are partially located in the terminal IRs. This would enable their autoregulation by Tpase binding.

Bibliography

  1. ↑ Doolittle WF, Kirkwood TB, Dempster MA . Selfish DNAs with self-restraint. - Nature: 1984 Feb 9-15, 307(5951);501-2 [PubMed:6320009] [DOI]


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