The photosynthetic bacterium responds to the transition from aerobiosis to anaerobic photosynthesis by increasing the expression of the photosynthesis genes. Mutants have been isolated based on their inability, following such a transition, to increase transcription of the operon encoding the apoproteins of the light-harvesting complex II. Mutant D5, a representative of one mutant class, described here, although remaining photosynthetically competent, produced only low levels of the photosynthetic spectral complexes. Complementation analysis revealed that either the gene for the photosynthesis response regulator or the gene encoding its cognate sensor kinase, was capable of rescuing this mutant. However, partial complementation of this mutant was achieved by placing additional copies of other defined genes from the cosmid library of We describe this effect in detail, attributable to the gene, which has been proposed to encode a histidine-kinase for the hydrogen uptake system in . The effect of HupT on the expression of the photosynthesis genes was mediated through PrrA and independent of a functioning hydrogen uptake system. Thus, we raise the possibility that HupT can participate in phosphorylation of the heterologous response regulator PrrA by so-called cross-talk and therefore partially compensate for the defect in the mutant described. The observation of cross-talk, together with the complementation analysis, allowed us to assign the original mutation to the gene; this was confirmed by DNA sequencing. Analysis of cross-talk in the wild-type, and genetic backgrounds suggested that besides kinase activity, PrrB may possess phosphatase activity toward PrrA. We also report the cloning, organization and structure of some of the genes from and construction of a Hup strain.


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