A missense mutation in rpoD results in an A-signalling defect in Myxococcus xanthus.
The Myxococcus xanthus asg genes (asgA, asgB, and asgC) are necessary for production of extracellular A-signal, which is thought to function as a cell-density signal. Previous analyses of the asgA and asgB genes suggest that they perform regulatory functions. In this work, we localized asgC to a region that contains genes homologous to rpsU, dnaG, and rpoD of the Escherichia coli macromolecular synthesis (MMS) operon. Surprisingly, asgC767 was found to be a mutant allele of rpoD, the gene encoding the major sigma factor of M. xanthus. The mutation in asgC767 results in a glutamate to lysine substitution at amino acid 598, which lies within conserved region 3.1 of the major sigma factors. Previous studies have shown that the asg mutants share a number of growth and developmental phenotypes. We found that A-signal restores developmental expression of an A-signal-dependent gene (omega 4521) in the asgC767 (rpoDEK598) mutant background in a manner similar to that seen in the asgA and asgB mutants. Because the asg mutants have very similar phenotypes and the asg genes encode proteins that appear to have regulatory functions, we hypothesize that the asg gene products function together in a regulatory pathway that is required for extracellular A-signal production.[1]References
- A missense mutation in rpoD results in an A-signalling defect in Myxococcus xanthus. Davis, J.M., Mayor, J., Plamann, L. Mol. Microbiol. (1995) [Pubmed]
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