No homologs of regulators (e.g. seqA, dam, hda) known in other bacteria

to control the mode of action of DnaA [64] have yet been identified in PCC9511. Still, one possible regulatory mechanism may involve ATP, Crenigacestat in vivo since it is a necessary co-factor transforming the inactive form of DnaA (DnaA-ADP) into its active form (DnaA-ATP), capable of initiating chromosome replication [65]. We hypothesize that the lowered expression levels of ATP synthase genes in HL+UV during the daytime, as seen both in microarray (for atpA, D, E, F, G and H; see above) and qPCR analyses (for atpD and atpH; see additional file 4: Fig. S3) could have caused

a decrease in intracellular ATP levels that might have also contributed to delayed DnaA induction activity in PCC9511. www.selleckchem.com/products/AZD1480.html Even if the lowered expression of dnaA is sufficient by itself to explain the observed S phase delay, it appears that UV exposure also check details strongly affected the expression of several (and possibly all) genes involved in cell division, including ftsZ and sepF, both encoding key components of the divisome [66]. This similar behavior suggests that the DNA replication and cell division machineries could be controlled by the same regulatory network, though the timing of maximal expression varies between genes (Fig. 6). SepF is thought to be involved in the polymerization and stability of FtsZ filaments. Marbouty and co-workers [32] showed in vitro that SepF binds to preassembled FtsZ polymers, suggesting that SepF is required only Venetoclax nmr after all the FtsZ protofilaments needed to make a Z-ring have been synthesized.

This hypothesis is consistent with the delay observed between the peaks of expression of ftsZ and sepF in both light conditions. DNA repair genes are activated under high light Another surprising result from this study is that UV exposure did not result in any significant upregulation of DNA repair genes (relative to HL conditions), including some which are known to be involved in repairing damage specifically induced by UV stress. This includes the phrA gene, which encodes an enzyme involved in repair (by photoreactivation) of the most frequent DNA lesions in response to UV, i.e. cyclobutane pyrimidine dimers (CPDs; [67]). Our results demonstrate that phrA is also strongly expressed under HL, with a pattern during the day that somewhat matched the irradiance curve, suggesting that the expression of this gene is strongly regulated by light. Recently, Osburne and co-workers [68] described a mutant of P. marinus MED4 exhibiting high resistance to UV stress.