TABLE 2.

Summary of genetic interactions involving Δtor1

Cells deleted for tor1⁺ were crossed with the indicated alleles. During vegetative growth, double mutant cells were phenotypically similar to the single mutant Δtor1 (None) or showed a synthetic lethal (SL) or sick (SS) interaction. If viable, double mutant strains were tested for their sensitivity to prolonged exposure to replication stress (HU, MMS, or CPT) and compared with the parental strains. The resulting double mutants showed negative genetic interactions (+) or strong negative genetic interactions (+++). Epistatic interactions were found with Δrad3 or Δrad17 in response to HU and MMS, as previously published (marked with an asterisk) (21).

Allele	Function	Untreated	Replication stress
Δrad3*	ATR checkpoint kinase, activates Chk1 and Cds1	None	Epistatis of rad3
Δrad17*	RFC-related checkpoint protein	None	Epistatis of rad17
Δchk1*	DNA damage checkpoint kinase	None	+
Δcds1*	DNA replication checkpoint kinase	None	+
Δmrc1*	Mediator of replication checkpoint 1	None	+
Δswi1	Replication fork protection complex subunit	None	+
Δswi3	Replication fork protection complex subunit	None	+
Δrad52	DNA recombination protein	SL	ND
Δrad51	RecA family recombinase	SL	ND
Δrqh1	RecQ type DNA helicase	None	+
Δmus81	Holliday junction resolvase	SS	+++
Δmms1	DNA repair protein in complex with mms22	SS	+++
Δmms22	DNA repair protein in complex with mms1	SS	+++
Δbrc1	BRCT domain protein	None	+++