(Downloading may take up to 30 seconds.
If the slide opens in your browser, select File -> Save As to save it.)
Click on image to view larger version.

Fig. 4. Genetic interactions between CCR4, the replication checkpoint and the DNA replication machinery. (A) Deletion of CCR4 is synthetic lethal with loss of RNR1 or RNR4. The diploid strains MT3802 (MATa/
ccr4
rnr4
) and MT3809 (MATa/
ccr4
rnr1
) were sporulated, dissected and genotyped (27 tetrads for ccr4
/rnr1
cross and 36 tetrads for ccr4
/rnr4
cross). Synthetic lethal interactions (ccr4
rnr1
or ccr4
rnr4
) were inferred from antibiotic resistance marker segregation (arrows). At least one isolate for each possible genotype is depicted. (B) ccr4
exacerbates the phenotypes of checkpoint and replication mutants. HU sensitivity of the indicated mutants was assessed by serial dilution on media containing indicated concentrations of HU, followed by growth for 3 days. Growth of pri1-M4 and ccr4
pri1-M4 (MT3799) strains was assessed on rich media, followed by incubation for 3 days at the indicated temperatures. (C) CCR4 acts independently of Rad53 and Mec1, but may act in concert with CHK1. The indicated checkpoint kinase mutations and strains were analyzed for HU sensitivity as above. (D) Quantitative assessment of sensitivity of the indicated strains to the indicated concentrations of HU was determined with a spiral plating system and CFU determined after 3-5 days growth.