Yeast histone H3 and H4 N termini function through different GAl1 regulatory elements to repress and activate transcription

• Published in: Proceedings of the National Academy of Sciences - PNAS Vol. 92; no. 12; pp. 5664 - 5668
• Main Authors: Wan, J.S. (University of California, Los Angeles, CA.), Mann, R.K, Grunstein, M
• Format: Journal Article
• Language: English
• Published: United States National Academy of Sciences of the United States of America 06-06-1995; National Acad Sciences; National Academy of Sciences
• Subjects: ADN RECOMBINADO; ADN RECOMBINE; Base Sequence; BETA GALACTOSIDASA; BETA GALACTOSIDASE; Binding sites; Chromatin; COMPOSICION QUIMICA; COMPOSITION CHIMIQUE; DNA Primers; Galactokinase - genetics; GENE; GENES; GENETICA; Genetics; GENETIQUE; HISTONAS; HISTONE; Histones; Histones - genetics; Molecular Sequence Data; Plasmids; Polymerase chain reaction; Promoter regions; Promoter Regions, Genetic; Proteins; Regulatory Sequences, Nucleic Acid; SACCHAROMYCES CEREVISIAE; Saccharomyces cerevisiae - genetics; Sequence Deletion; TATA Box; Transcription, Genetic; Yeast; Yeasts
• ISSN: 0027-8424; 1091-6490
• DOI: 10.1073/pnas.92.12.5664

Previous work has shown that N-terminal deletions of yeast histone H3 cause a 2- to 4-fold increase in the induction of GAL1 and a number of other genes involved in galactose metabolism. In contrast, deletions at the H4 N terminus cause a 10- to 20-fold decrease in the induction of these same GAL genes. However, H3 and H4 N-terminal deletions each decrease PHO5 induction only 2- to 4-fold. To define the GAL1 gene regulatory elements through which the histone N termini activate or repress transcription, fusions were made between GAL1 and PHO5 promoter elements attached to a beta-galactosidase reporter gene. We show here that GAL1 hyperactivation caused by the H3 N-terminal deletion delta4-15 is linked to the upstream activation sequence. Conversely, the relative decrease in GAL1 induction caused by the H4 N-terminal deletion delta4-28 is linked to the downstream promoter which contains the TATA element. These data indicate that the H3 N terminus is required for the repression of the GAL1 upstream element, whereas the H4 N terminus is required for the activation of the GAL1 downstream promoter element