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Genetics, Vol 145, 923-934, Copyright © 1997
INVESTIGATIONS |
The Role of Sas2, an Acetyltransferase Homologue of Saccharomyces cerevisiae, in Silencing and ORC Function
A. E. Ehrenhofer-Murray, D. H. Rivier and J. Rine
Division of Genetics, Department of Molecular and Cell Biology, University of California, Berkeley, California 94720
Silencing at the cryptic mating-type loci HML and HMR of Saccharomyces cerevisiae requires regulatory sites called silencers. Mutations in the Rap1 and Abf1 binding sites of the HMR-E silencer (HMRa-e**) cause the silencer to be nonfunctional, and hence, cause derepression of HMR. Here, we have isolated and characterized mutations in SAS2 as second-site suppressors of the silencing defect of HMRa-e**. Silencing conferred by the removal of SAS2 (sas2{Delta}) depended upon the integrity of the ARS consensus sequence of the HMR-E silencer, thus arguing for an involvement of the origin recognition complex (ORC). Restoration of silencing by sas2{Delta} required ORC2 and ORC5, but not SIR1 or RAP1. Furthermore, sas2{Delta} suppressed the temperature sensitivity, but not the silencing defect of orc2-1 and orc5-1. Moreover, sas2{Delta} had opposing effects on silencing of HML and HMR. The putative Sas2 protein bears similarities to known protein acetyltransferases. Several models for the role of Sas2 in silencing are discussed.
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