Title: | "A histone variant, Htz1p, and a Sir1p-like protein, Esc2p, mediate silencing at HMR" |
Address: | "Unit on Chromatin and Transcription, NICHD/NIH, Bethesda, Maryland 20892, USA" |
DOI: | 10.1016/s1097-2765(00)00076-9 |
ISSN/ISBN: | 1097-2765 (Print) 1097-2765 (Linking) |
Abstract: | "Silencing at HMR requires silencers, and one of the roles of the silencer is to recruit Sir proteins. This work focuses on the function of Sir1p once it is recruited to the silencer. We have generated mutants of Sir1p that are recruited to the silencer but are unable to silence, and we have utilized these mutants to identify four proteins, Sir3p, Sir4p, Esc2p, and Htz1p, that when overexpressed, restored silencing. The isolation of Sir3p and Sir4p validated this screen. Molecular analysis suggested that Esc2p contributed to silencing in a manner similar to Sir1p and probably helped recruit or stabilize the other Sir proteins, while Htz1p present at HMR assembled a specialized chromatin structure necessary for silencing" |
Keywords: | "Alleles Chromatin/physiology/ultrastructure DNA-Binding Proteins Fungal Proteins/*genetics/*metabolism *Gene Silencing Genes, Fungal Histones/*metabolism Mating Factor Mutagenesis Peptides/genetics Saccharomyces cerevisiae/*genetics/growth & development/m;" |
Notes: | "MedlineDhillon, N Kamakaka, R T eng Research Support, U.S. Gov't, P.H.S. 2000/11/25 Mol Cell. 2000 Oct; 6(4):769-80. doi: 10.1016/s1097-2765(00)00076-9" |