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Transient promoter formation: a new feedback mechanism for regulation of IS 911 transposition
Author(s) -
DuvalValentin Guy,
Normand Christophe,
Khemici Vanessa,
Marty Brigitte,
Chandler Michael
Publication year - 2001
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1093/emboj/20.20.5802
Subject(s) - transposase , transposition (logic) , transposable element , biology , insertion sequence , tn10 , inverted repeat , genetics , p element , microbiology and biotechnology , gene , mutant , computer science , genome , artificial intelligence
IS 911 transposition involves a free circular transposon intermediate where the terminal inverted repeat sequences are connected. Transposase synthesis is usually driven by a weak promoter, p IRL , in the left end (IRL). Circle junction formation creates a strong promoter, p junc , with a −35 sequence located in the right end and the −10 sequence in the left. p junc assembly would permit an increase in synthesis of transposase from the transposon circle, which would be expected to stimulate integration. Insertion results in p junc disassembly and a return to the low p IRL ‐ driven transposase levels. We demonstrate that p junc plays an important role in regulating IS 911 transposition. Inactivation of p junc strongly decreased IS 911 transposition when transposase was produced in its natural configuration. This novel feedback mechanism permits transient and controlled activation of integration only in the presence of the correct (circular) intermediate. We have also investigated other members of the IS 3 and other IS families. Several, but not all, IS 3 family members possess p junc equivalents, underlining that the regulatory mechanisms adopted to fine‐tune transposition may be different.