4.6 Article

MioC and GidA proteins promote cell division in E-coil

期刊

FRONTIERS IN MICROBIOLOGY
卷 6, 期 -, 页码 -

出版社

FRONTIERS MEDIA SA
DOI: 10.3389/fmicb.2015.00516

关键词

mioC; gidA; bacterial cell division; bacterial cell cycle; oriC; FIS; replication initiation; ymgF

资金

  1. National Institutes of Health (NIH) [R01GM102679]
  2. NIH [DP1-CA174424, P30 AI036211, P30 CAl25123, S10 RR024574]

向作者/读者索取更多资源

The well-conserved genes surrounding the E coli replication origin, mioC and gidA, do not normally affect chromosome replication and have little known function. We report that mioC and gidA mutants exhibit a moderate cell division inhibition phenotype. Cell elongation is exacerbated by a fis deletion, likely owing to delayed replication and subsequent cell cycle stress. Measurements of replication initiation frequency and origin segregation indicate that mioC and gidA do not inhibit cell division through any effect on oriC function. Division inhibition is also independent of the two known replication/cell division checkpoints, SOS and nucleoid occlusion. Complementation analysis indicates that mioC and gidA affect cell division in trans, indicating their effect is at the protein level. Transcriptome analysis by RNA sequencing showed that expression of a cell division septum component, YmgF, is significantly altered in mioC and gidA mutants. Our data reveal new roles for the gene products of gidA and mioC in the division apparatus, and we propose that their expression, cyclically regulated by chromatin remodeling at oriC, is part of a cell cycle regulatory program coordinating replication initiation and cell division.

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