The yeast meiotic activator IME1 stimulates transcription of many early meiotic genes. These genes share a 5' sequence called URS1. URS1 sites function as repression sites in cells that lack IME1; we show here that URS1 sites are weak activation sequences in cells that express IME1. Repression through URS1 sites is known to depend upon the URS1-binding protein UME6. We have identified a UME6 allele (previously called rim16-12) that causes a defect in IME1-dependent activation of meiotic genes but not in repression through URS1 sites. In contrast, a ume6 null mutation causes defects in both IME1-dependent activation and in repression through URS1 sites. A LexA-UME6 fusion protein is an IME1-dependent transcriptional activator, whereas a LexA-UME6 fusion carrying the rim16-12 substitution cannot activate transcription. These findings argue that IME1 activates meiotic genes by converting UME6 from a negative regulator to a positive regulator; the rim16-12 mutant protein is defective in conversion to a positive regulator.

• PMID: 7760793
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Journal Article | Research Support, Non-U.S. Gov't | Research Support, U.S. Gov't, P.H.S.

Authors

Bowdish KS, Yuan HE, Mitchell AP

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