SetB: an integral membrane protein that affects chromosome segregation in Escherichia coli

Authors


E-mail k-marians@ski.mskcc.org; Tel. (+1) 212 639 5890; Fax (+1) 212 717 3627.

Summary

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.

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