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Volume 272, Number 7, Issue of February 14, 1997 pp. 4613-4622
©1997 by The American Society for Biochemistry and Molecular Biology, Inc.

Genomic Footprinting of Mig1p in the MAL62 Promoter
BINDING IS DEPENDENT UPON CARBON SOURCE AND COMPETITIVE WITH THE Mal63p ACTIVATOR

(Received for publication, September 10, 1996, and in revised form, November 25, 1996)

Jianfan Wang , Oxana Sirenko and Richard Needleman

From the Department of Biochemistry and Molecular Biology, Wayne State University School of Medicine, Detroit, Michigan 48201

Mig1p inhibits gene expression in glucose by binding the Cyc8p (Ssn6p)-Tup1p repressor to the promoter of glucose-repressible genes. While the binding properties of Mig1p have been studied in vitro and the ability of Mig1p-Cyc8p (Ssn6p)-Tup1p to repress has been studied in vivo, no experiments have measured the effect of a carbon source on the in vivo binding of Mig1p or the effect of bound MIg1p on activator occupancy of the upstream activation sequence (UAS). To obtain this information, we used genomic footprinting to investigate glucose repression of MAL62, a gene that is also regulated by the Mal63p activator. These experiments show that two interrelated mechanisms are involved in the glucose repression of MAL62: 1) competition between the Mal63p activator and Mig1p for DNA binding and 2) modulation of Mig1p binding by the carbon source. Mig1p affects basal MAL62 expression in the absence of Mal63p by binding to a site in the MAL62 promoter and affects Mal63p-dependent synthesis by also inhibiting the access of Mal63p to site 1 in the UASMAL. The binding of Mig1p is increased in glucose and decreased in nonrepressing sugars, but the increased binding in glucose is not due to an increase in the levels of Mig1p.


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