TY - JOUR
T1 - Yeast Gal11 protein mediates the transcriptional activation signal of two different transacting factors, Gal4 and general regulatory factor I/repressor/activator site binding protein 1/translation upstream factor
AU - Nishizawa, M.
AU - Suzuki, Y.
AU - Nogi, Y.
AU - Matsumoto, K.
AU - Fukasawa, T.
PY - 1990
Y1 - 1990
N2 - 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 a-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 (GFRI)/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 Ga14 and GFRI/RAP1/TUF, when the respective binding site is situated at the naturally occurring distance from the TATA box.
AB - 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 a-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 (GFRI)/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 Ga14 and GFRI/RAP1/TUF, when the respective binding site is situated at the naturally occurring distance from the TATA box.
KW - DNA-binding proteins
KW - Mating
KW - Protein-protein interaction
KW - Transcriptional regulation
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U2 - 10.1073/pnas.87.14.5373
DO - 10.1073/pnas.87.14.5373
M3 - Article
C2 - 2196565
AN - SCOPUS:0025142739
SN - 0027-8424
VL - 87
SP - 5373
EP - 5377
JO - Proceedings of the National Academy of Sciences of the United States of America
JF - Proceedings of the National Academy of Sciences of the United States of America
IS - 14
ER -