GAL11 was first identified as a gene required for full expression of some of the galactose-inducible genes in the yeast Saccharomyces cerevisiae. A null mutation within the GAL11 locus causes defects in mating, growth on nonfermentable carbon sources, and sporulation of gal11 homozygotes. The mating defect was observed only in MATα gal11 strains. Northern hybridization analysis revealed that a gal11 mutation impaired transcription of α-specific genes (MFα1 and STE3) but not of an α-specific gene (STE2). Furthermore, this mutation reduced expression of the MATα locus, suggesting that a deficiency in MATα1 protein is responsible for the reduced expression of α-specific genes. Since general regulatory factor I (GRFI)/repressor/activator site binding protein 1 (RAP1)/translation upstream factor (TUF) is believed to be an activator of MATα expression, we examined whether PYK1, which is known to be regulated by GRFI/RAP1/TUF, is also affected by the gal11 mutation. It was determined that the level of PYK1 message was significantly lowered by the mutation. The requirement for functional GAL11 in transcriptional activation was bypassed when either the upstream activating sequence of galactose-inducible genes or of PYK1 was placed very close to the TATA box, suggesting that one of the Gal11 protein functions is to mediate the activation signal of Gal4 and GRFI/RAP1/TUF, when the respective binding site is situated at the naturally occurring distance from the TATA box. (.
|Proceedings of the National Academy of Sciences of the United States of America
|Published - 1990
ASJC Scopus subject areas