Glucose repression and derepression mediated by H3 and H4 tails.
Juan Jose Infante, Rhiannon Biddick, Chris Tachibana, Elton T. Young
Biochemistry, University of Washington, Box 357350, Seattle, WA, 98195-7350, United States
Chromatin remodeling and transcription activation of the ADH2 promoter after glucose depletion requires the transcription factor Adr1. Adr1 binding and limited remodeling occur without transcription in a strain lacking the histone deacetylases Rpd3 and Hda1, where the histone N-termini are hyperacetylated. We have extended this observation to other Adr1-regulated genes and have shown that Snf1, an AMP-dependent protein kinase homolog, is necessary for binding of Adr1 to hyperacetylated chromatin, although the known Snf1 substrate, H3-Ser10, is apparently not involved. The histone acetylase Gcn5 is important for ADH2 derepression, but apparently plays no role in Adr1 binding to chromatin. Confirming the importance of modification of the histone tails, deletion of H3 or H4 amino termini allows Adr1 to bind chromatin and partially relieves repression of an Adr1-dependent reporter gene. Therefore, both H3 and H4 amino termini are required to prevent Adr1 from binding chromatin. As in the deacetylase mutant, a second step after chromatin binding is apparently necessary for efficient transcription because the relief from repression is lower than would be predicted from the amount of Adr1 bound to the promoter. Monitoring ADH2 expression in the histone tail mutants after a shift to very low glucose indicated that H3 affects early steps in derepression and H4 is required for maintenance of high-level transcription. Thus, the tails play a role in both repression and derepression.
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