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 | + | 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== | |
| − | + | {{Reflist|32em}} | |
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| + | {{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
