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The S-phase cyclin clb5 promotes replication initiation efficiency in r-RNA.

Jan Huizinga

The regulation of replication origins is necessary for complete genome duplication, but it is unclear how origin activation affects the cellular response to replication stress. At the replication fork barrier (RFB), the rRNA gene of budding yeast (rDNA) undergoes tandem repeat formation and replication fork arrest, resulting in DNA double-strand breaks (DSBs), genome instability, and copy number changes. Here, we show that rDNA stability is promoted by the S-phase cyclin Clb5. Clb5 is required for replication initiation in rDNA, but its absence reduced this efficiency. However, it had little impact on the number of replication forks arrested at the RFB, indicating that the converging fork's arrival is delayed and forks are more stably arrested at the RFB. Removal of CLB5 had no impact on DSB rDNA instability was caused by homologous recombination-dependent repair at the RFB. As a result, rDNA instability at arrested forks at the RFB may be DSB-independent but recombination-dependent. The lack of Fob1, which is in charge of fork arrest at the RFB, did not completely suppress the rDNA instability in clb5. As a result, Clb5 establishes the correct distance between active replication origins and reduces the amount of time DNA polymerases must travel, which may lessen Fob1-independent DNA damage.