Regulation of Bacillus subtilis glutamine synthetase gene expression by the product of the glnR gene.
Transcription of the Bacillus subtilis gene coding of glutamine synthetase ( glnA) is regulated by the nitrogen source. The glnA gene lies in an operon in which it is preceded by an open reading frame with the potential to encode a polypeptide of approximately 16,000 Mr. We have now shown that this open reading frame is utilized in vivo, that its product (GlnR) acts as a diffusible, negative regulator of gln transcription, and that GlnR is likely to be a DNA-binding protein. Certain mutations in glnR, including a large, in-frame deletion and a start codon mutation, led to high-level constitutivity of the operon; other mutations caused low-level constitutivity. These latter mutations, which affected the C terminus of GlnR, seemed to disrupt response to the nitrogen source without eliminating the ability of GlnR to bind to DNA. Wild-type GlnR by itself, however, did not impose nitrogen-dependent regulation; such regulation also required the product of glnA. A model is presented in which glutamine synthetase monitors the availability of nitrogen and imposes negative regulation by interaction with or modification of GlnR.[1]References
- Regulation of Bacillus subtilis glutamine synthetase gene expression by the product of the glnR gene. Schreier, H.J., Brown, S.W., Hirschi, K.D., Nomellini, J.F., Sonenshein, A.L. J. Mol. Biol. (1989) [Pubmed]
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