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Histone H3 N‐terminal mutations allow hyperactivation of the yeast GAL1 gene in vivo.
Author(s) -
Mann R.K.,
Grunstein M.
Publication year - 1992
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1002/j.1460-2075.1992.tb05408.x
Subject(s) - biology , histone h3 , histone , nucleosome , genetics , histone code , gene , microbiology and biotechnology
Recent work has shown that the yeast histone H4 N‐terminus, while not essential for viability, is required for repression of the silent mating loci and activation of GAL1 and PHO5 promoters. Because histone H3 shares many structural features with histone H4 and is intimately associated with H4 in the assembled nucleosome, we asked whether H3 has similar functions. While the basic N‐terminal domain of H3 is found to be non‐essential (deletion of residues 4–40 of this 135 amino acid protein allows viability), its removal has only a minor effect on mating. Surprisingly, both deletions (of residues 4–15) and acetylation site substitutions (at residues 9, 14 and 18) within the N‐terminus of H3 allow hyperactivation of the GAL1 promoter as well as a number of other GAL4‐regulated genes including GAL2, GAL7 and GAL10. To a limited extent glucose repression is also alleviated by H3 N‐terminal deletions. Expression of another inducible promoter, PHO5, is shown to be relatively unaffected. We conclude that the H3 and H4 N‐termini have different functions in both the repression of the silent mating loci and in the regulation of GAL1.