The genes encoding succinate dehydrogenase , the specific components of the 2-oxoglutarate dehydrogenase complex (ODH, E1o and E2o; ) and succinyl-CoA synthetase form a cluster containing two promoters at 16.3 min in the chromosome of . The gene encoding the lipoamide dehydrogenase component of both the 2-oxoglutarate and pyruvate dehydrogenase complexes (E3; ) is the distal gene of another cluster containing two promoters located at 2.7 min: . The responses of the suc and promoters to different environmental conditions and to regulator defects were investigated with appropriate fusions, in order to understand how expression of the genes is co-regulated with other genes in the cluster and with expression. Expression from the promoter was repressed by IHF and partially activated by σ but it was not regulated by ArcA, FNR, CRP, FruR or Fis, and not repressed by glucose or anaerobiosis, indicating that the well-established catabolite and anaerobic repression of ODH synthesis is imposed elsewhere. In contrast, the promoter was repressed by both glucose (via a CRP-independent mechanism) and anaerobiosis (mediated by ArcA), and activated by Fis, but it was not regulated by FNR, FruR, IHF or σ. These observations support the view that transcription of the genes is primarily initiated and regulated at the upstream promoter, and that the promoter is independently co-regulated with (primarily by ArcA-mediated repression) rather than with Direct evidence for co-transcription of the entire region from was obtained by detecting a 10 kb transcript in and mutants, but not in the parental strains. Three RNaseIII-specific processing sites, which contribute to the extreme instability of the readthrough transcript, were identified in the intergenic region. Other sites of endonuclease processing were located by interpreting the patterns of transcript subfragments observed in Northern blotting.


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