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

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    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC212837/
    Permanent Link
    https://doi.org/10.1128/jb.167.1.35-43.1986
    http://hdl.handle.net/11603/13119
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    • UMBC Biological Sciences Department
    • UMBC Department of Marine Biotechnology
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    Author/Creator
    Schreier, Harold J.
    Sonenshein, Abraham L.
    Date
    1986-07-01
    Type of Work
    9 pages
    Text
    journal articles
    Citation of Original Publication
    H. 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.167.1.35-43.1986
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    This 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.
    Subjects
    beta-galactosidase by Bacillus subtilis
    glutamine synthetase (GS)
    glnA-lacZ fusion
    Abstract
    Expression 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.


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    Albin O. Kuhn Library & Gallery
    University of Maryland, Baltimore County
    1000 Hilltop Circle
    Baltimore, MD 21250
    www.umbc.edu/scholarworks

    Contact information:
    Email: scholarworks-group@umbc.edu
    Phone: 410-455-3021


    If you wish to submit a copyright complaint or withdrawal request, please email mdsoar-help@umd.edu.