Complex regulation of the Bacillus subtilis aconitase gene

The roles of the CcpC, CodY, and AbrB proteins in regulation of the Bacillus subtilis aconitase (citB) gene were found to be distinct and to vary with the conditions and phase of growth. CcpC, a citrate-inhibited repressor that is the primary factor regulating citB expression in minimal-glucose-glutamine medium, also contributed to repression of citB during exponential-phase growth in broth medium. A null mutation in codY had no effect on citB expression during growth in minimal medium even when combined with ccpC and abrB mutations. However, a codY mutation slightly relieved repression during exponential growth in broth medium and completely derepressed citB expression when combined with a ccpC mutation. An abrB mutation led to decreased expression of citB during stationary phase in both broth and minimal medium. All three proteins bound in vitro to specific and partially overlapping sites within the citB regulatory region. Interaction of CcpC and CodY with the citB promoter region was partially competitive.     

Nrg1 functions as a global transcriptional repressor of glucose-repressed genes through its direct binding to the specific promoter regions

Nrg1 is a zinc finger protein involved in the glucose repression of several glucose-repressed genes such as STA1, SUC2, and GAL1. Although the molecular details of the Nrg1-mediated repression of STA1 have been partly characterized, it still remains largely unknown how Nrg1 regulates these multiple target genes. In this study, we show that Nrg1 mediates the glucose repression of SUC2 and HXT2 through its direct binding to the specific promoter regions; it binds to the −404 to −360 region of the SUC2 promoter and the −957 to −810 region of the HXT2 promoter. Nrg1 also interacts with the −380 to −250 region of the PCK1 promoter, suggesting that it might also contribute to the PCK1 repression. In addition, ChIP assays confirmed that Nrg1 associated with specific promoter regions of these glucose-repressed genes in vivo. Analysis of the DNA fragments to which it binds indicates that Nrg1 may recognize T/ACCCC sequence within the promoters of these glucose-repressed genes as well as in its own promoter. Collectively, our findings indicate that Nrg1 mediates the glucose repression of multiple genes through its direct binding to the specific promoter regions.