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

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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.
 
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==
 
==Bibliography==
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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]