Yeast histone H3 and H4 N termini function through different GAL1 regulatory elements to repress and activate transcription.
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 delta 4-15 is linked to the upstream activation sequence. Conversely, the relative decrease in GAL1 induction caused by the H4N-terminal deletion delta 4-28 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 H4N terminus is required for the activation of the GAL1 downstream promoter element.
Wan
J S
JS
Department of Biological Chemistry, School of Medicine, University of California, Los Angeles 90095, USA.
Mann
R K
RK
Grunstein
M
M
D001483:Base Sequence; D017931:DNA Primers; D005686:Galactokinase / Q000235:genetics; D006657:Histones / Q000235:genetics*; D008969:Molecular Sequence Data; D011401:Promoter Regions, Genetic; D012045:Regulatory Sequences, Nucleic Acid; D012441:Saccharomyces cerevisiae / Q000235:genetics*; D017384:Sequence Deletion; D016385:TATA Box; D014158:Transcription, Genetic
D017931:DNA Primers; D006657:Histones; D005686:Galactokinase