par Bahassi, El Mustapha 
;Salmon, M A;Van Melderen, Laurence ;Bernard, P;Couturier, Martine
Référence Molecular microbiology, 15, 6, page (1031-1037)
Publication Publié, 1995-03
;Salmon, M A;Van Melderen, Laurence ;Bernard, P;Couturier, Martine Référence Molecular microbiology, 15, 6, page (1031-1037)
Publication Publié, 1995-03
Article révisé par les pairs
| Résumé : | The ccd locus of the F plasmid codes for two gene products, CcdA and CcdB, which contribute to the plasmid's high stability by post-segregational killing of plasmid-free bacteria. Like the quinolones, the CcdB protein is a poison of the DNA-topoisomerase II complexes, while CcdA acts as an antidote against CcdB. In addition to these poison-antipoison properties, the CcdA and CcdB proteins act together at transcription level to repress their own synthesis. In this work, we have isolated, in vivo, and characterized several non-killer CcdB mutants. All missense mutations which inactivate CcdB killer activity are located in the region coding for the last three C-terminal residues. However, the resulting mutant CcdB proteins retain their autoregulatory properties. We conclude that the last three C-terminal residues of CcdB play a key role in poisoning but are not involved in repressor formation. |
