Abstract
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.
Highlights
In all cells, DNA replication and cell division are temporally coordinated to maintain a one-toone relationship between genome and cell duplication
MioC and GidA Promote Cell Division without Affecting Replication Initiation We have shown that mioC and gidA mutants have a reduced capacity to divide, which is exacerbated by a fis deletion
(3) Division inhibition did not involve SOS induction, which could have resulted from DNA damage caused by replication defects, as shown by an absence of PsulA-GFP expression in triple mutant PmioC PgidA fis cells and by normal sulA expression in PmioC and PgidA strains by transcription profiling
Summary
DNA replication and cell division are temporally coordinated to maintain a one-toone relationship between genome and cell duplication. Pioneering work by the Helmstetter lab (Cooper and Helmstetter, 1968) indicated that the bacterial cell cycle might be controlled solely by the frequency and timing of replication initiation This idea stemmed from synchronized cell experiments, which showed that in E. coli B/r strains the periods of DNA replication and septum development were relatively constant (∼40 and 20 min, respectively) with the remainder of the cell cycle defined as a flexible pre-initiation “B” period (Dix and Helmstetter, 1973). It was hypothesized that cell division was triggered by an unknown event occurring at the end of the replication period, presumably replication of an essential cell division gene (Dix and Helmstetter, 1973; Den Blaauwen et al, 1999). Supporting this view, replication termination and cell division occur at the same cell location (Bates and Kleckner, 2005; Wang et al, 2005), and there is even some sharing of machinery between the two processes (e.g., FtsK translocase, Wang et al, 2005, 2006; Burton et al, 2007)
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