Abstract
The SSN6-TUP1 protein complex represses transcription of diversely regulated genes in the yeast Saccharomyces cerevisiae. Here we present evidence that MIG1, a zinc-finger protein in the EGR1/Zif268 family, recruits SSN6-TUP1 to glucose-repressed promoters. DNA-bound LexA-MIG1 represses transcription of a target gene in glucose-grown cells, and repression requires SSN6 and TUP1. We also show that MIG1 and SSN6 fusion proteins interact in the two-hybrid system. Unexpectedly, we found that LexA-MIG1 activates transcription strongly in an ssn6 mutant and weakly in a tup1 mutant. Finally, LexA-MIG1 does not repress transcription in glucose-deprived cells, and MIG1 is differentially phosphorylated in response to glucose availability. We suggest a role for phosphorylation in regulating repression.
Publication types
-
Research Support, U.S. Gov't, P.H.S.
MeSH terms
-
Bacterial Proteins / genetics
-
Base Sequence
-
DNA-Binding Proteins / genetics*
-
DNA-Binding Proteins / metabolism
-
Fungal Proteins / genetics*
-
Fungal Proteins / metabolism
-
Gene Expression Regulation, Fungal*
-
Glucose / metabolism
-
Models, Genetic
-
Molecular Sequence Data
-
Nuclear Proteins*
-
Phosphorylation
-
Protein Binding
-
Recombinant Fusion Proteins / metabolism
-
Repressor Proteins*
-
Saccharomyces cerevisiae / genetics*
-
Saccharomyces cerevisiae Proteins*
-
Serine Endopeptidases*
-
Transcription, Genetic*
Substances
-
Bacterial Proteins
-
CYC8 protein, S cerevisiae
-
DNA-Binding Proteins
-
Fungal Proteins
-
LexA protein, Bacteria
-
MIG1 protein, S cerevisiae
-
Nuclear Proteins
-
Recombinant Fusion Proteins
-
Repressor Proteins
-
Saccharomyces cerevisiae Proteins
-
TUP1 protein, S cerevisiae
-
Serine Endopeptidases
-
Glucose