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Suppression of a dominant G protein β‐subunit mutation in yeast by Gα protein expression
Author(s) -
Zhang Meng,
Tipper Donald J.
Publication year - 1993
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1111/j.1365-2958.1993.tb01740.x
Subject(s) - biology , saccharomyces cerevisiae , protein subunit , signal transduction , mutant , microbiology and biotechnology , null allele , mating type , mutation , allele , phenotype , yeast , gene , genetics
Summary SCG1/GPA1, STE4 , and STE18 encode the α, β and λ components of the G protein involved in mating pheromone signal transduction in Saccharomyces cerevisiae. Responses, including G1 arrest and expression of genes such as FUS1 , are activated by βλ, which is negatively controlled by α(GDP), We previously demonstrated that overexpression of Scg1 suppresses responses to α factor and that expression of certain hybrids between Scg1 and mammalian Gα proteins has the same effect and also suppresses growth arrest in an scg1 ‐null mutant. Effects were attributed to sequestration of βλ. We now show that effects on growth rate, morphology and FUS1 expression are consistent with this model. The STE4 HPL allele causes dominant activation of the response pathway, and is presumed to encode a β subunit insensitive to control by α(GDP). Scg1 overexpression suppresses the growth arrest due to STE4 HPL ; normal α‐factor responses and fertility are restored. A model based on sequestration of βγ reconciles this result with the apparent paradox that the same level of Scg1 overexpression inhibits responses and mating in wild‐type cells. A Gαi hybrid also restores growth and allows inefficient mating in the STE HPL strain.