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Journal of Bacteriology, June 1999, p. 3341-3350, Vol. 181, No. 11
Department of Biochemistry, University of
Connecticut Health Center, Farmington, Connecticut 06032
Received 4 January 1999/Accepted 24 March 1999
Bacillus subtilis spores break their metabolic dormancy
through a process called germination. Spore germination is triggered by
specific molecules called germinants, which are thought to act by
binding to and stimulating spore receptors. Three homologous operons,
gerA, gerB, and gerK, were
previously proposed to encode germinant receptors because inactivating
mutations in those genes confer a germinant-specific defect in
germination. To more definitely identify genes that encode germinant
receptors, we isolated mutants whose spores germinated in the novel
germinant D-alanine, because such mutants would likely
contain gain-of-function mutations in genes that encoded preexisting
germinant receptors. Three independent mutants were isolated, and in
each case the mutant phenotype was shown to result from a single
dominant mutation in the gerB operon. Two of the mutations
altered the gerBA gene, whereas the third affected the
gerBB gene. These results suggest that gerBA
and gerBB encode components of the germinant receptor.
Furthermore, genetic interactions between the wild-type
gerB and the mutant gerBA and gerBB
alleles suggested that the germinant receptor might be a complex
containing GerBA, GerBB, and probably other proteins. Thus, we propose
that the gerB operon encodes at least two components of a
multicomponent germinant receptor.
0021-9193/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
Isolation and Characterization of Mutations in
Bacillus subtilis That Allow Spore Germination in the Novel
Germinant D-Alanine
*
Corresponding author. Mailing address: Department of
Biochemistry, University of Connecticut Health Center, Farmington,
Conn. 06032. Phone: (860) 679-2607. Fax: (860) 679-3408. E-mail:
setlow{at}sun.uchc.edu.
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