Affiliation:
1. Department of Biological Sciences, Auburn University, Auburn, Alabama 36849-5407
2. School of Dentistry, Molecular Biology Institute, and Dental Research Institute, University of California—Los Angeles, Los Angeles, California 90095-1668
Abstract
ABSTRACT
In bacteria with multiple sets of chemotaxis genes, the deletion of homologous genes or even different genes in the same operon can result in disparate phenotypes.
Myxococcus xanthus
is a bacterium with multiple sets of chemotaxis genes and/or homologues. It was shown previously that
difA
and
difE
, encoding homologues of the methyl-accepting chemoreceptor protein (MCP) and the CheA kinase, respectively, are required for
M. xanthus
social gliding (S) motility and development. Both
difA
and
difE
mutants were also defective in the biogenesis of the cell surface appendages known as extracellular matrix fibrils. In this study, we investigated the roles of the CheW homologue encoded by
difC
, a gene at the same locus as
difA
and
difE
. We showed that
difC
mutations resulted in defects in
M. xanthus
developmental aggregation, sporulation, and S motility. We demonstrated that
difC
is indispensable for wild-type cellular cohesion and fibril biogenesis but not for pilus production. We further illustrated the ectopic complementation of a
difC
in-frame deletion by a wild-type
difC
. The identical phenotypes of
difA
,
difC
, and
difE
mutants are consistent and supportive of the hypothesis that the Dif chemotaxis homologues constitute a chemotaxis-like signal transduction pathway that regulates
M. xanthus
fibril biogenesis and S motility.
Publisher
American Society for Microbiology
Subject
Molecular Biology,Microbiology
Cited by
45 articles.
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