Altered regulation of the glnA gene in glutamine synthetase mutants of Bacillus subtilis

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dc.contributor.authorSchreier, Harold J.
dc.contributor.authorSonenshein, Abraham L.
dc.date.accessioned2019-03-21T19:43:10Z
dc.date.available2019-03-21T19:43:10Z
dc.date.issued1986-07-01
dc.description.abstractExpression of beta-galactosidase by Bacillus subtilis strains carrying transcriptional fusions of the glnA promoter region to the Escherichia coli lacZ gene was found to be regulated by the nitrogen source in glnA+ strains. The pattern of regulation was the same as that for glutamine synthetase (GS); the strongest repression was seen when glutamine was present in the medium. To see this regulation it was necessary for the fusion to be in low copy number, a condition achieved by forcing integration into the chromosome. We constructed a strain carrying a deletion mutation (glnA200) that removes part of the 5' end of the glnA structural gene. This strain did not produce any detectable GS activity or measurable GS antigen. We introduced this mutation and other glnA mutations (glnA73, glnA93, and glnA100) into strains carrying glnA-lacZ fusions. When the strains were grown with glutamine as the nitrogen source, beta-galactosidase activity was found to be derepressed. These results indicate that functional glnA gene product is required for the regulation of transcription from the glnA promoter. This supports the conclusion of our previous studies of the B. subtilis glnA gene cloned in E. coli. Additional factors may also be involved in glnA control. In particular, our results suggest that a 500-base-pair sequence of DNA between the promoter region and the start of the glnA structural gene plays a role in regulation; strains carrying this region within the glnA-lacZ fusion and unable to produce functional GS exhibited only partially derepressed beta-galactosidase levels when grown in the presence of glutamine.en_US
dc.description.sponsorshipThis work was supported by Public Health Service research grant GM-19168 from the National Institutes of Health to A.L.S. and a postdoctoral fellowship (F32 GM-09430) from the National Institutes of Health to H.J.S.en_US
dc.description.urihttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC212837/en_US
dc.format.extent9 pagesen_US
dc.genrejournal articlesen_US
dc.identifierdoi:10.13016/m2j3tb-o334
dc.identifier.citationH. J. Schreier and A. L. Sonenshein, Altered regulation of the glnA gene in glutamine synthetase mutants of Bacillus subtilis, J Bacteriol. 1986 Jul; 167(1): 35–43, https://doi.org/10.1128/jb.167.1.35-43.1986en_US
dc.identifier.urihttps://doi.org/10.1128/jb.167.1.35-43.1986
dc.identifier.urihttp://hdl.handle.net/11603/13119
dc.language.isoen_USen_US
dc.publisherAmerican Society for Microbiologyen_US
dc.relation.isAvailableAtThe University of Maryland, Baltimore County (UMBC)
dc.relation.ispartofUMBC Department of Marine Biotechnology
dc.relation.ispartofUMBC Biological Sciences Department
dc.rightsThis item is likely protected under Title 17 of the U.S. Copyright Law. Unless on a Creative Commons license, for uses protected by Copyright Law, contact the copyright holder or the author.
dc.subjectbeta-galactosidase by Bacillus subtilisen_US
dc.subjectglutamine synthetase (GS)en_US
dc.subjectglnA-lacZ fusionen_US
dc.titleAltered regulation of the glnA gene in glutamine synthetase mutants of Bacillus subtilisen_US
dc.typeTexten_US

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