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MioC and GidA proteins promote cell division in E. coli
Mark Lies1, Bryan J Visser2, Mohan C Joshi1
1Molecular and Human Genetics, Baylor College of Medicine Houston, TX, USA.
Frontiers in Microbiology
|June 16, 2015
Summary
Mutations in mioC and gidA genes cause cell division inhibition in E. coli, independent of replication origin function. These genes play a novel role in the cell division apparatus.
Area of Science:
- Microbiology
- Molecular Biology
- Genetics
Background:
- The genes mioC and gidA, located near the E. coli replication origin, have poorly understood functions.
- While conserved, their roles in chromosome replication and cell division are not well-defined.
Purpose of the Study:
- To investigate the function of mioC and gidA in E. coli.
- To determine the mechanism by which mioC and gidA influence cell division and its coordination with DNA replication.
Main Methods:
- Construction and analysis of mioC and gidA mutants in E. coli.
- Phenotypic analysis including cell elongation and division inhibition.
- Assessment of replication initiation frequency and origin segregation.
- Investigation of known cell cycle checkpoints (SOS and nucleoid occlusion).
- Complementation analysis to determine the mode of action (cis/trans).
- Transcriptome analysis using RNA sequencing.
Main Results:
- mioC and gidA mutants display moderate cell division inhibition and increased cell elongation, particularly when combined with a fis deletion.
- The cell division defect is not due to effects on oriC function or known checkpoints (SOS, nucleoid occlusion).
- Complementation analysis confirmed that mioC and gidA act in trans, suggesting protein-level function.
- RNA sequencing revealed significant alterations in the expression of YmgF, a cell division septum component, in mioC and gidA mutants.
Conclusions:
- The gene products of gidA and mioC have previously unrecognized roles in the cell division machinery.
- Their expression, potentially regulated by chromatin remodeling at oriC, is proposed to be part of a cell cycle program coordinating DNA replication initiation and cell division.
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