The Rap1p/Gcr1p complex is required for efficient expression of
glycolytic and ribosomal protein genes. Only the glycolytic promoters
require both a functional Gcr1p binding site in DNA (the CT box) and the
auxiliary factor Gcr2p. Relief from these ancillary requirements can be
accomplished by either a change in chromosomal position or bypass
mutations in Gcr1p. Interestingly, bypass of the Gcr2 - growth
defect in complete medium is abolished in minimal medium. Further
investigation of this phenomenon has revealed that Gcr2 -
bypass lesions in GCR1 uncouple activation of glycolytic genes
from the stringent response of ribosomal protein genes. We will also
present evidence that this differential regulation of the two main
classes of Rap1p target promoters is accomplished through changes in the
phosphorylation state of Gcr1p, which we have shown is altered
dramatically in the presence of Gcr2p. Gcr1p therefore appears to
coordinate the transcriptional response to changes in nutritional
environment.
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