Ptc1 acts downstream of the MEKK, Ssk2. Deletion of PTC1 exacerbated growth defects due to overexpression of SSK2ΔN, consistent with its role as a negative regulator. The wild type and a ptc1Δ strain were transformed with pSSK2ΔN, a multicopy plasmid expressing the hyperactive MEKK allele, SSK2ΔN, under regulation of the GAL1 promoter, or the empty vector pYES2. Growth on galactose conferred only a slight defect in the wild type but was lethal in a ptc1Δ strain. Growth of strains on selective medium (SM) containing galactose was assessed after 3 days at 30°C.