Kraxner, Kim Julia;
Polen, Tino;
Baumgart, Meike;
Bott, Michael
The conserved actinobacterial transcriptional regulator FtsR controls expression of ftsZ and further target genes and influences growth and cell division in Corynebacterium glutamicum
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Media type:
E-Article
Title:
The conserved actinobacterial transcriptional regulator FtsR controls expression of ftsZ and further target genes and influences growth and cell division in Corynebacterium glutamicum
Contributor:
Kraxner, Kim Julia;
Polen, Tino;
Baumgart, Meike;
Bott, Michael
Published:
Springer Science and Business Media LLC, 2019
Description:
<jats:title>Abstract</jats:title><jats:sec>
<jats:title>Background</jats:title>
<jats:p>Key mechanisms of cell division and its regulation are well understood in model bacteria such as <jats:italic>Escherichia coli</jats:italic> and <jats:italic>Bacillus subtilis.</jats:italic> In contrast, current knowledge on the regulation of cell division in <jats:italic>Actinobacteria</jats:italic> is rather limited. FtsZ is one of the key players in this process, but nothing is known about its transcriptional regulation in <jats:italic>Corynebacterium glutamicum,</jats:italic> a model organism of the <jats:italic>Corynebacteriales</jats:italic>.</jats:p>
</jats:sec><jats:sec>
<jats:title>Results</jats:title>
<jats:p>In this study, we used DNA affinity chromatography to search for transcriptional regulators of <jats:italic>ftsZ</jats:italic> in <jats:italic>C. glutamicum</jats:italic> and identified the Cg1631 protein as candidate, which was named FtsR. Both deletion and overexpression of <jats:italic>ftsR</jats:italic> caused growth defects and an altered cell morphology. Plasmid-based expression of native <jats:italic>ftsR</jats:italic> or of homologs of the pathogenic relatives <jats:italic>Corynebacterium diphtheriae</jats:italic> and <jats:italic>Mycobacterium tuberculosis</jats:italic> in the Δ<jats:italic>ftsR</jats:italic> mutant could at least partially reverse the mutant phenotype. Absence of <jats:italic>ftsR</jats:italic> caused decreased expression of <jats:italic>ftsZ</jats:italic>, in line with an activator function of FtsR. In vivo crosslinking followed by affinity purification of FtsR and next generation sequencing of the enriched DNA fragments confirmed the <jats:italic>ftsZ</jats:italic> promoter as in vivo binding site of FtsR and revealed additional potential target genes and a DNA-binding motif. Analysis of strains expressing <jats:italic>ftsZ</jats:italic> under control of the gluconate-inducible <jats:italic>gntK</jats:italic> promoter revealed that the phenotype of the Δ<jats:italic>ftsR</jats:italic> mutant is not solely caused by reduced <jats:italic>ftsZ</jats:italic> expression, but involves further targets.</jats:p>
</jats:sec><jats:sec>
<jats:title>Conclusions</jats:title>
<jats:p>In this study, we identified and characterized FtsR as the first transcriptional regulator of FtsZ described for <jats:italic>C. glutamicum</jats:italic>. Both the absence and the overproduction of FtsR had severe effects on growth and cell morphology, underlining the importance of this regulatory protein. FtsR and its DNA-binding site in the promoter region of <jats:italic>ftsZ</jats:italic> are highly conserved in <jats:italic>Actinobacteria</jats:italic>, which suggests that this regulatory mechanism is also relevant for the control of cell division in related <jats:italic>Actinobacteria</jats:italic>.</jats:p>
</jats:sec>