Table 2.

Perturbagen penetrance and genetic epistasis

Perturbagen	Percentage of cells plated that formed colonies in the presence of α factor		Suppression of slow-growth phenotypes
	Dextrose	Galactose	GAL–STE4	STE11ΔN
pVT21	<0.5	<0.5	−	−
pep1(I)	<0.5	60  ±  2	−	−
pep2(I)	<0.5	69  ±  3	+	+
pep3(C)	<0.5	90  ±  7	+	−
pep4(C)	<0.5	71  ±  9	+	+
pep5(C)	<0.5	6  ±  2	−	−
orf1	<0.5	55  ±  9	−	−
orf2	<0.5	19  ±  10	−	−
orf3	<0.5	18  ±  4	−	−
orf4	<0.5	23  ±  4	+	−
orf5	<0.5	65  ±  4	+	+
orf6	<0.5	47  ±  6	−	−
orf7	<0.5	34  ±  9	−	−
orf8	<0.5	65  ±  9	+	−
orf9	<0.5	9  ±  4	−	−
orf10	<0.5	59  ±  5	−	−
orf11	<0.5	40  ±  4	−	−

Expression of the GAL-STE4 and STE11ΔN alleles resulted in slow growth rather than complete growth arrest when coexpressed with the parental plasmid pVT21 (both the GAL–STE4 and STE11ΔN alleles caused complete growth arrest in the absence of pVT21). This slow growth may have resulted from limiting levels of the GAL4 transcription factor because binding sites for GAL4p were present in pVT21, its derivatives, and the GAL–STE4 and STE11ΔN expression plasmids. Failure of some perturbagens (e.g., orf2) to suppress growth defects caused by the GAL–STE4 and STE11ΔN alleles was likely caused by the generally low penetrance of these perturbagens. However, this failure also could result from inhibition of targets that act at the same point as or upstream of STE4p or from an inability of particular perturbagens to inhibit these specific dominant alleles.