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 l-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 H4 N-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 H4 N terminus is required for the activation of the GAL1 downstream promoter element.