title: Regulation of Bacillus subtilis aprE expression by glnA through inhibition of scoC and sigma(D)-dependent degR expression.
abstract: Expression of the gene for the extracellular alkaline protease (aprE) of Bacillus subtilis is subject to regulation by many positive and negative regulators. We have found that aprE expression was increased by disruption of the glutamine synthetase gene glnA. The increase in aprE expression was attributed to a decreased in expression of scoC, which encodes a negative regulator of aprE expression. The glnA effect on scoC expression was abolished by further disruption of tnrA, indicating that aprE expression is under global regulation through TnrA. In the scoC background, however, aprE expression was decreased by glnA deletion, and it was shown that the decrease was due to a defect in positive regulation by DegU. Among the genes that affect aprE expression through DegU, the expression of degR, encoding a protein that stabilizes phosphorylated DegU, was inhibited by glnA deletion. It was further shown that the decrease in degR expression by glnA deletion was caused by inhibition of the expression of sigD, encoding the sigma(D) factor, which is required for degR expression. In accordance with these findings, the expression levels of aprE-lacZ in glnA scoC degR and scoC degR strains were identical. These results led us to conclude that glnA deletion brings about two effects on aprE expression, i.e., a positive effect through inhibition of scoC expression and a negative effect through inhibition of degR expression, with the former predominating over the latter.
authors.affiliation: Institute of Oceanic Research and Development, Tokai University, Orido 3-20-1, Shimizu-ku, Shizuoka 424-8610, Japan.
authors.forename: Sadanobu
authors.initials: S
authors.lastname: Abe
authors.forename: Ayako
authors.initials: A
authors.lastname: Yasumura
authors.forename: Teruo
authors.initials: T
authors.lastname: Tanaka
mesh_terms: D000818:Animals; D019677:Artificial Gene Fusion; D001412:Bacillus subtilis / Q000502:physiology*; D001426:Bacterial Proteins / Q000037:antagonists & inhibitors* / Q000096:biosynthesis* / Q000235:genetics / Q000502:physiology; D001483:Base Sequence; D017353:Gene Deletion; D015964:Gene Expression Regulation, Bacterial; D017930:Genes, Reporter; D005974:Glutamate-Ammonia Ligase / Q000235:genetics / Q000502:physiology*; D026901:Membrane Transport Proteins / Q000096:biosynthesis*; D008969:Molecular Sequence Data; D046329:Octodon; D011401:Promoter Regions, Genetic; D012097:Repressor Proteins / Q000235:genetics / Q000502:physiology; D012808:Sigma Factor / Q000502:physiology; D014157:Transcription Factors / Q000037:antagonists & inhibitors*; D001616:beta-Galactosidase / Q000235:genetics / Q000378:metabolism
chemical_list: C088074:AprE protein, Bacteria; D001426:Bacterial Proteins; D026901:Membrane Transport Proteins; D012097:Repressor Proteins; C101458:ScgR protein, Bacillus subtilis; C442131:ScoC protein, Bacillus subtilis; D012808:Sigma Factor; D014157:Transcription Factors; D001616:beta-Galactosidase; C081173:glutamine synthetase I; D005974:Glutamate-Ammonia Ligase