Contributed equally to the work.
Canonical and non-canonical EcfG sigma factors control the general stress response in Rhizobium etli
Article first published online: 28 OCT 2013
© 2013 The Authors. MicrobiologyOpen published by John Wiley & Sons Ltd.
This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
Volume 2, Issue 6, pages 976–987, December 2013
How to Cite
MicrobiologyOpen 2013; 2(6): 976–987
- Issue published online: 6 DEC 2013
- Article first published online: 28 OCT 2013
- Manuscript Accepted: 23 SEP 2013
- Manuscript Revised: 16 SEP 2013
- Manuscript Received: 27 JUL 2013
- Belgian Science Policy Office
- Research Council of the KU Leuven. Grant Number: GOA/011/2008
- Fund for Scientific Research-Flanders. Grant Number: G.0412.10
- ECF sigma factor;
- general stress response;
A core component of the α-proteobacterial general stress response (GSR) is the extracytoplasmic function (ECF) sigma factor EcfG, exclusively present in this taxonomic class. Half of the completed α-proteobacterial genome sequences contain two or more copies of genes encoding σEcfG-like sigma factors, with the primary copy typically located adjacent to genes coding for a cognate anti-sigma factor (NepR) and two-component response regulator (PhyR). So far, the widespread occurrence of additional, non-canonical σEcfG copies has not satisfactorily been explained. This study explores the hierarchical relation between Rhizobium etli σEcfG1 and σEcfG2, canonical and non-canonical σEcfG proteins, respectively. Contrary to reports in other species, we find that σEcfG1 and σEcfG2 act in parallel, as nodes of a complex regulatory network, rather than in series, as elements of a linear regulatory cascade. We demonstrate that both sigma factors control unique yet also shared target genes, corroborating phenotypic evidence. σEcfG1 drives expression of rpoH2, explaining the increased heat sensitivity of an ecfG1 mutant, while katG is under control of σEcfG2, accounting for reduced oxidative stress resistance of an ecfG2 mutant. We also identify non-coding RNA genes as novel σEcfG targets. We propose a modified model for GSR regulation in R. etli, in which σEcfG1 and σEcfG2 function largely independently. Based on a phylogenetic analysis and considering the prevalence of α-proteobacterial genomes with multiple σEcfG copies, this model may also be applicable to numerous other species.