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Budding yeast possesses a checkpoint-dependent mechanism of delaying G 1  progression in response to UV and ionizing radiation DNA damage. We have shown that after a pulse of DNA damage in G 1  with the alkylating agent MMS, there is also a MEC1 -,  RAD53 -, and  RAD9 -dependent delay in G 1 . This delay occurs at or before Start, as the MMS-treated cells do not bud, remain sensitive to α-factor, and have low CLN1  and  CLN2  transcript levels for a longer time than untreated cells. We further show that MMS directly and reversibly down-regulates  CLN1  and  CLN2  transcript levels. The initial drop in  CLN  transcript levels in MMS is not RAD53  dependent, but the kinetics of reaccumulation of CLN  messages as cells recover from the damage is faster in rad53-11  cells than in wild type cells. This is not an indirect effect of faster progression through G 1 , because  CLN transcripts reaccumulate faster in  rad53-11  mutants arrested in G 1  as well. In addition, the recovery of  CLN  mRNA levels can be also hastened by a  SWI6  deletion or by overexpression of the truncated Swi4 (Swi4-t) that lacks the carboxy-terminal domain through which Swi4 associates with Swi6. This indicates that both Rad53 and Swi6 are negative regulators of CLN  expression after DNA damage. Finally, Swi6 undergoes an MMS-inducible,  RAD53 -dependent phosphorylation in G 1 cells, and Rad53, immunoprecipitated from MMS-treated cells, phosphorylates Swi6 in vitro. On the basis of these observations, we suggest that the Rad53-dependent phosphorylation of Swi6 may delay the transition to S phase by inhibiting  CLN  transcription.

genes and development

Rad53-dependent phosphorylation of Swi6 and down-regulation of CLN1 andCLN2 transcription occur in response to DNA damage inSaccharomyces cerevisiae