Affiliation:
1. Department of Molecular Biology and Microbiology, Tufts University School of Medicine, Boston, Massachusetts 02111, USA.
Abstract
A mutation (gltR24) that allows Bacillus subtilis glutamate synthase (gltAB) gene expression in the absence of its positive regulator, GltC, was identified. Cloning and sequencing of the gltR gene revealed that the putative gltR product belongs to the LysR family of transcriptional regulators and is thus related to GltC. A null mutation in gltR had no effect on gltAB expression under any environmental condition tested, suggesting that gltR24 is a gain-of-function mutation. GltR24-dependent transcription of gltAB, initiated at the same base pair as GltC-dependent transcription, was responsive to the nitrogen source in the medium and required the integrity of sequences upstream of the gltAB promoter that are also necessary for GltC-dependent expression. Expression of the gltC gene, transcribed divergently from gltA from an overlapping promoter, was not affected by GltR. Both wild-type GltR and GltR24 negatively regulated their own expression. The gltR gene was mapped to 233 degrees on the B. subtilis chromosome, very close to the azlB locus.
Publisher
American Society for Microbiology
Subject
Molecular Biology,Microbiology
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