PMID: 2107531Feb 25, 1990Paper

A mutation in the Zn-finger of the GAL4 homolog LAC9 results in glucose repression of its target genes

Nucleic Acids Research
P KugerK D Breunig

Abstract

The transcriptional activator LAC9, a GAL4 homolog of Kluyveromyces lactis which mediates lactose and galactose-dependent activation of genes involved in the utilization of these sugars can also confer glucose repression to those genes. Here we report on the isolation and characterization of LAC9-2, an allele which encodes a glucose-sensitive activator in contrast to the one previously cloned. A single amino acid exchange of leu-104 to tryptophan is responsible for the glucose-insensitive phenotype. The mutation is located within the Zn-finger-like DNA binding domain which is highly conserved between LAC9 and GAL4. Glucose repression is also eliminated by duplication of the LAC9-2 allele. The data indicate that LAC9 is a limiting factor for beta-galactosidase gene expression under all growth conditions and that glucose reduces the activity of the activator.

References

Dec 1, 1977·Proceedings of the National Academy of Sciences of the United States of America·F SangerA R Coulson
Aug 25, 1988·Nucleic Acids Research·T D Webster, R C Dickson
Apr 1, 1987·Proceedings of the National Academy of Sciences of the United States of America·M Johnston, J Dover
Dec 1, 1985·Proceedings of the National Academy of Sciences of the United States of America·K Sreekrishna, R C Dickson
May 15, 1984·European Journal of Biochemistry·P Eraso, J M Gancedo
Jan 1, 1961·Cold Spring Harbor Symposia on Quantitative Biology·B MAGASANIK

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Citations

Jul 1, 1992·Proceedings of the National Academy of Sciences of the United States of America·M S Lamphier, M Ptashne
Nov 18, 1997·European Journal of Biochemistry·J WeirichK D Breunig

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