The PpsR protein is a regulator of redox-dependent photosystem development in purple phototrophic bacteria. In contrast to most species, Rhodopseudomonas palustris contains two ppsR genes. We show that the inactivation of each of the R. palustris strain CGA009 ppsR genes results in an elevated level of formation of the photosystem under dark aerobic conditions. Absorption spectra of the two PpsR mutants revealed qualitative and quantitative differences in light-harvesting peak amplitude increases. A sequence difference in the helix-turn-helix DNA binding motif of PpsR2 (Arg 439 to Cys) between R. palustris strains CEA001 and CGA009 is shown to be a natural polymorphism that does not inactivate the repressor activity of the protein. To evaluate which photosynthesis genes are regulated by the two PpsR proteins, transcriptome profiles of the CGA009 and PpsR mutant strains were analyzed in microarray experiments. Transcription of most but not all photosystem genes was derepressed in the mutant strains to levels consistent with the in vivo absorption spectra, mathematical analyses of peak shapes and amplitudes, reaction center protein levels, and real-time PCR of selected mRNAs. Closely spaced PpsR binding motif repeats were identified 5' of genes that were derepressed in the transcriptome analysis of PpsR mutants. This work shows that both the PpsR1 and PpsR2 proteins from R. palustris strain CGA009 function as oxygen-responsive transcriptional repressors.

The tmRNA-SmpB system releases ribosomes stalled on truncated mRNAs and tags the nascent polypeptides to target them for proteolysis. In many species, mutations that disrupt tmRNA activity cause defects in growth or development. In Caulobacter crescentus cells lacking tmRNA activity there is a delay in the initiation of DNA replication, which disrupts the cell cycle. To understand the molecular basis for this phenotype, 73 C. crescentus proteins were identified that are tagged by tmRNA under normal growth conditions. Among these substrates, proteins involved in DNA replication, recombination, and repair were overrepresented, suggesting that misregulation of these factors in the absence of tmRNA activity might be responsible for the delay in initiation of DNA replication. Analysis of the tagging sites within these substrates revealed a conserved nucleotide motif 5 of the tagging site, which is required for wild-type tmRNA tagging.bacterial cell cycle ͉ proteolysis ͉ trans-translation

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