RME1 is a zinc-finger protein homolog that functions as a repressor of the meiotic activator IME1. RME1 is unusual among yeast repressors in two respects: it acts over a considerable distance (2 kbp) and it can activate transcription from a binding site separated from its natural flanking region. To identify genes required for RME1 to exert repression, we have selected mutants with improved RME1-dependent activation. One rare mutant was defective in RME1-dependent repression of an artificial reporter gene as well as the native IME1 gene. The mutation permits sporulation of a/a diploids, which express RME1 from its natural promoter, and of a/alpha diploids constructed to express RME1 from the GAL1 promoter. The mutation also causes temperature-sensitive growth and a methionine or cysteine requirement. Analysis of a complementing genomic clone indicates that the mutation lies in a known essential gene, RGR1. Prior studies have indicated a functional relationship between RGR1 and SIN4 (also called TSF3); we have found that a sin4 null mutation also causes a defect in RME1-dependent repression and a methionine or cysteine requirement. The rgr1 and sin4 mutations do not cause a reduction of RME1 polypeptide levels. The defect in RME1-dependent repression may result from effects of sin4 and, presumably, rgr1 on chromatin structure.

• PMID: 7851756
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Journal Article | Research Support, Non-U.S. Gov't | Research Support, U.S. Gov't, P.H.S.

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Covitz PA, Song W, Mitchell AP

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