A histone variant, Htz1p, and a Sir1p-like protein, Esc2p, mediate silencing at HMR.

摘要: Silencing at HMR requires silencers, and one of the roles silencer is to recruit Sir proteins. This work focuses on function Sir1p once it recruited silencer. We have generated mutants that are but unable silence, we utilized these identify four proteins, Sir3p, Sir4p, Esc2p, Htz1p, when overexpressed, restored silencing. The isolation Sir3p Sir4p validated this screen. Molecular analysis suggested Esc2p contributed silencing in a manner similar probably helped or stabilize other while Htz1p present assembled specialized chromatin structure necessary for