The following buy Emricasan step of the MMR process, i.e. DNA excision, is ensured in E. coli by

several genes, including recJ, which encodes a single-stranded DNA-specific exonuclease and the xseAB operon, which encodes the two subunits of the exodeoxyribonuclease VII [72]. Surprisingly, homologs of these genes can be found in the genomes of the low light-adapted Prochlorococcus ecotypes, but not in high light adapted ecotypes, including MED4 [3]. Thus, even though putative homologs of enzymes involved in DNA resynthesis (the last step of MMR [72]) are present in MED4, including SSB, which has been implicated in the repair of single strand breaks, and several DNA ligases (in addition to the universal, error-free

replicative DNA polymerase III, or Pol III, which is also involved in this process), biochemical studies are needed to determine whether MutS is associated with an MMR-like system in HL-adapted P. marinus strains or if this system is absent in these organisms. Expression patterns of the umuC gene, encoding the subunit C of the UmuD’2C error-prone DNA polymerase V (Pol V), indicate that DNA translesion synthesis (TLS) reactions, used to bypass lesions selleck products in DNA templates on which Pol III usually stalls, occur in PCC9511 [73]. The umuC gene expression increased during the G1 phase with a peak at noon and was downregulated during the S phase. Interestingly, in HL+UV conditions, its expression

level remained high during the entire period of S blockage. Posttranslational Evodiamine activation of Pol V requires the presence of RecA nucleoprotein filaments bound to ssDNA in order to generate its catalytically active form [74]. One can therefore speculate that, even though umuC expression was upregulated in the middle of the day under HL+UV conditions, the transcriptional repression of recA during that time may have delayed activation of Pol V. As a result, stalled replication forks may have taken longer to be rescued [75], providing another possible cause for the delay in S maximum observed under HL+UV. The umuCD-dependent cell cycle checkpoint model proposed for E. coli [57] may thus be applicable to P. marinus PCC9511. While the NER (and possibly MMR) pathway is mainly active during the G1 phase, Prochlorococcus cells seem to activate another DNA repair system after the initiation of chromosome replication, namely the selleck homologous recombination pathway that acts on double strand breaks. In this process, RuvA and RuvB, form a complex that promotes branch migration of Holliday junctions, then the endonuclease RuvC resolves the Holliday junctions by introducing nicks into DNA strands [76].