| Literature DB >> 14617174 |
Olivier Espeli1, Pearl Nurse, Cindy Levine, Chong Lee, Kenneth J Marians.
Abstract
SetB was identified as a high-copy suppressor of the partition defect of a mutation in parC, encoding one of the subunits of topoisomerase IV. Deletion of this integral inner membrane protein causes a delay in chromosome segregation, whereas its overproduction causes nucleoid disintegration and stretching, leading to a cell division defect. setB deletion mutants also exhibit a synthetic phenotype when combined with mutations that delete the C-terminal motor domain of the septal ring protein FtsK. SetB localizes in the cell as a helix and interacts with MreB, the bacterial actin homologue, which also forms a helix. These observations suggest that there may be a link between chromosome segregation and cellular infrastructure.Entities:
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Year: 2003 PMID: 14617174 DOI: 10.1046/j.1365-2958.2003.03736.x
Source DB: PubMed Journal: Mol Microbiol ISSN: 0950-382X Impact factor: 3.501