Difference between revisions of "General Information/Control of transposition activity"
Jump to navigation
Jump to search
| (4 intermediate revisions by the same user not shown) | |||
| 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 | + | 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. |
| − | |||
| − | |||
| − | |||
==Bibliography== | ==Bibliography== | ||
| − | < | + | {{Reflist|32em}} |
| + | <br/> | ||
| + | <hr> | ||
| + | {{TnPedia}} | ||
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
