AUTHOR=Lies Mark , Visser Bryan J. , Joshi Mohan C. , Magnan David , Bates David 

TITLE=MioC and GidA proteins promote cell division in E. coli

JOURNAL=Frontiers in Microbiology

VOLUME=6

YEAR=2015

URL=https://www.frontiersin.org/journals/microbiology/articles/10.3389/fmicb.2015.00516

DOI=10.3389/fmicb.2015.00516

ISSN=1664-302X

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