Jump to content

General Information/Control of transposition activity: Difference between revisions

From TnPedia
No edit summary
m Text replacement - "<ref><pubmed>" to "<ref>{{#"
Line 1: Line 1:
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>{{#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.
==Bibliography==
==Bibliography==
{{Reflist|32em}}
{{Reflist|32em}}

Revision as of 20:02, 27 May 2025

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. {{#6320009</pubmed>