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Mol Microbiol. 2001 Feb;39(3):765-80.

Identification and characterization of spdR mutations that bypass the BsgA protease-dependent regulation of developmental gene expression in Myxococcus xanthus.

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1
Department of Microbiology, University of Colorado Health Sciences Center, 4200 East 9th Ave., Campus Box B-175, Denver, CO 80262, USA.

Abstract

The BsgA protease of Myxococcus xanthus is an intracellular protease closely related to the Lon protease of Escherichia coli. BsgA is required for normal levels of developmentally induced gene expression. In this report, we describe the identification of mutations that suppress the developmental defect of bsgA mutants. These mutations localized to the spdR gene (suppressor protease deficiency regulator) that appears to play a role in the regulation of early developmental gene expression. Mutations in spdR fully restored the ability of a bsgA mutant to form fruiting bodies and spores and, with one exception, restored the expression of several development-specific lacZ fusions. spdR mutants exhibited characteristic phenotypic properties including increased expression of the development-specific tps gene during vegetative growth, formation of fruiting bodies and spores on semi-rich nutrient medium and completion of starvation-induced development in a shorter time period than wild-type strains. The spdR locus was cloned and sequenced and found to encode a member of the NtrC family of two-component transcriptional regulators. One interpretation of these data is that SpdR acts, directly or otherwise, to regulate developmental gene expression negatively and that the BsgA protease is required to relieve this inhibitory effect at the onset of development. However, Western immunoblot analysis indicated that SpdR is present at a relatively constant level during growth and early development in both wild-type and BsgA protease-deficient cells. This finding suggests that BsgA does not function to degrade SpdR at the onset of development.

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