Molecular oxygen levels regulate Sinorhizobium meliloti cell division through a FixJ-dependent transcription control mechanism
Rhizobia infect the roots of host legumes and induce formation of nitrogen-fixing nodules, where nitrogenase genes are inducibly expressed by micro-aerobic signals. FixL/FixJ is an oxygen signal sensing system that is unique to rhizobia. FixL monitors molecular oxygen levels and phosphorylates the r...
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Veröffentlicht in: | Biochemical and biophysical research communications 2022-07, Vol.614, p.132-137 |
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Sprache: | eng |
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Zusammenfassung: | Rhizobia infect the roots of host legumes and induce formation of nitrogen-fixing nodules, where nitrogenase genes are inducibly expressed by micro-aerobic signals. FixL/FixJ is an oxygen signal sensing system that is unique to rhizobia. FixL monitors molecular oxygen levels and phosphorylates the response regulator FixJ, thereby regulating downstream gene expression. The cell division of rhizobia is regulated by a phosphorylation relaying cascade that includes the transcription factors CtrA, GcrA, and DnaA. In Sinorhizobium meliloti the expression of these proteins is regulated by NtrX, which affects cell division. In the present work, by analyzing the cell division phenotypes and gene expression patterns of S. meliloti fixJ and ntrX mutants, we found that S. meliloti cell division is regulated by oxygen gas levels. Under normal conditions, FixJ induced NtrX and DnaA expression, but repressed CtrA and GcrA expression. In contrast, under hypoxic conditions, phosphorylated FixJ specifically bound to gene promoter regions to directly induce CtrA and GcrA expression, but to repress DnaA expression. Our findings reveal that molecular oxygen levels regulate S. meliloti cell division by a FixJ-dependent transcription control mechanism.
•Sinorhizobium meliloti cell division is regulated by oxygen gas levels.•Under normal conditions, FixJ induced NtrX and DnaA expression, but repressed CtrA and GcrA expression.•Under hypoxic conditions, phosphorylated FixJ specifically regulates the expression of CtrA, GcrA and DnaA. |
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ISSN: | 0006-291X 1090-2104 |
DOI: | 10.1016/j.bbrc.2022.05.006 |