Fig 5. Orc5-binding site of Rrm3 is required for cell viability and tolerance to HU and MMS in the absence of Mrc1/Tof1 but not in the absence of Rad5, Rad51, Rdh54 or Mph1.

(A) Residues 186–212 of Rrm3 are required for mrc1Δ viability. Diploids heterozygous for mrc1Δ and rrm3Δ mutations were transformed with plasmids expressing N-terminal truncations of Rrm3 and 100 meiotic products that grew on SC-Leu media, indicating the presence of the plasmid-borne RRM3 alleles, were genotyped. Absence of meiotic products that grew on SC-Leu-Trp-His indicates synthetic lethality between the rrm3 allele and mrc1Δ. (B) Absence of residues 186–212 of Rrm3 increases sensitivity of the tof1Δ mutant to HU and MMS. (C-G) Requirement of the ATPase/helicase activity of Rrm3, but not the Orc5-binding site between residues 186–212, for suppression of HU and MMS hypersensitivity of rdh54Δ, rad51Δ, rad5Δ and mph1Δ mutants. RRM3 is not required in the rad54Δ mutant for tolerating HU or MMS.