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

Lies M, Visser BJ, Joshi MC, Magnan D, Bates D - Front Microbiol (2015)

Bottom Line: The well-conserved genes surrounding the E. coli replication origin, mioC and gidA, do not normally affect chromosome replication and have little known function.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.

View Article: PubMed Central - PubMed

Affiliation: Molecular and Human Genetics, Baylor College of Medicine Houston, TX, USA.

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.

No MeSH data available.


Related in: MedlinePlus

Transcription in theoriCregion. The minimal oriC (white box) and surrounding genes are shown, with transcription direction indicated by arrows. Binding sites for DnaA (blue boxes) and SeqA (orange boxes) overlap mioC and gidA promoters, respectively. Relative transcription in wildtype and gidA and mioC promoter mutants, as determined by RNA-sequencing is shown (height of red lines indicate relative reads per base pair).
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Figure 1: Transcription in theoriCregion. The minimal oriC (white box) and surrounding genes are shown, with transcription direction indicated by arrows. Binding sites for DnaA (blue boxes) and SeqA (orange boxes) overlap mioC and gidA promoters, respectively. Relative transcription in wildtype and gidA and mioC promoter mutants, as determined by RNA-sequencing is shown (height of red lines indicate relative reads per base pair).

Mentions: One possible connection between replication initiation and cell division is through activated expression of a cell division regulator gene near the replication origin, oriC. The very highly conserved gidA gene, which is located immediately leftward of oriC (Figure 1), was previously implicated in cell division via a cell filamentation phenotype in gidA (glucose inhibited division) deletion mutants when grown in glucose-containing media (Von Meyenburg and Hansen, 1980). The mechanism of the division defect in gidA mutants is unclear. Wild-type gidA, also known as mnmG, encodes a protein that in combination with MnmE is involved in modification of specific tRNA molecules, (Bregeon et al., 2001; Moukadiri et al., 2009). This tRNA modification may be important to prevent deleterious ribosomal frameshift mutations. However, comparison of mnmE and gidA (mnmG) mutant phenotypes indicates that GidA has additional functions outside tRNA modificiation (Bregeon et al., 2001). The other well-conserved gene flanking the replication origin is mioC, located immediately rightward of oriC (Figure 1). mioC encodes a protein that has been implicated in biotin synthesis in vitro (Birch et al., 2000), but mioC mutants do not require biotin for growth in rich or minimal medium (D.B., unpublished). Thus, MioC protein has no established biological function.


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

Lies M, Visser BJ, Joshi MC, Magnan D, Bates D - Front Microbiol (2015)

Transcription in theoriCregion. The minimal oriC (white box) and surrounding genes are shown, with transcription direction indicated by arrows. Binding sites for DnaA (blue boxes) and SeqA (orange boxes) overlap mioC and gidA promoters, respectively. Relative transcription in wildtype and gidA and mioC promoter mutants, as determined by RNA-sequencing is shown (height of red lines indicate relative reads per base pair).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4446571&req=5

Figure 1: Transcription in theoriCregion. The minimal oriC (white box) and surrounding genes are shown, with transcription direction indicated by arrows. Binding sites for DnaA (blue boxes) and SeqA (orange boxes) overlap mioC and gidA promoters, respectively. Relative transcription in wildtype and gidA and mioC promoter mutants, as determined by RNA-sequencing is shown (height of red lines indicate relative reads per base pair).
Mentions: One possible connection between replication initiation and cell division is through activated expression of a cell division regulator gene near the replication origin, oriC. The very highly conserved gidA gene, which is located immediately leftward of oriC (Figure 1), was previously implicated in cell division via a cell filamentation phenotype in gidA (glucose inhibited division) deletion mutants when grown in glucose-containing media (Von Meyenburg and Hansen, 1980). The mechanism of the division defect in gidA mutants is unclear. Wild-type gidA, also known as mnmG, encodes a protein that in combination with MnmE is involved in modification of specific tRNA molecules, (Bregeon et al., 2001; Moukadiri et al., 2009). This tRNA modification may be important to prevent deleterious ribosomal frameshift mutations. However, comparison of mnmE and gidA (mnmG) mutant phenotypes indicates that GidA has additional functions outside tRNA modificiation (Bregeon et al., 2001). The other well-conserved gene flanking the replication origin is mioC, located immediately rightward of oriC (Figure 1). mioC encodes a protein that has been implicated in biotin synthesis in vitro (Birch et al., 2000), but mioC mutants do not require biotin for growth in rich or minimal medium (D.B., unpublished). Thus, MioC protein has no established biological function.

Bottom Line: The well-conserved genes surrounding the E. coli replication origin, mioC and gidA, do not normally affect chromosome replication and have little known function.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.

View Article: PubMed Central - PubMed

Affiliation: Molecular and Human Genetics, Baylor College of Medicine Houston, TX, USA.

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.

No MeSH data available.


Related in: MedlinePlus