Moretti P, Shore D
Department of Microbiology, College of Physicians & Surgeons of Columbia University, New York, New York 10032, USA.
Mol Cell Biol. 2001 Dec;21(23):8082-94. doi: 10.1128/MCB.21.23.8082-8094.2001.
Initiation of transcriptional silencing at mating type loci and telomeres in Saccharomyces cerevisiae requires the recruitment of a Sir2/3/4 (silent information regulator) protein complex to the chromosome, which occurs at least in part through its association with the silencer- and telomere-binding protein Rap1p. Sir3p and Sir4p are structural components of silent chromatin that can self-associate, interact with each other, and bind to the amino-terminal tails of histones H3 and H4. We have identified a small region of Sir3p between amino acids 455 and 481 that is necessary and sufficient for association with the carboxyl terminus of Rap1p but not required for Sir complex formation or histone binding. SIR3 mutations that delete this region cause a silencing defect at HMR and telomeres. However, this impairment of repression is considerably less than that displayed by Rap1p carboxy-terminal truncations that are defective in Sir3p binding. This difference may be explained by the ability of the Rap1p carboxyl terminus to interact independently with Sir4p, which we demonstrate by in vitro binding and two-hybrid assays. Significantly, the Rap1p-Sir4p two-hybrid interaction does not require Sir3p and is abolished by mutation of the carboxyl terminus of Rap1p. We propose that both Sir3p and Sir4p can directly and independently bind to Rap1p at mating type silencers and telomeres and suggest that Rap1p-mediated recruitment of Sir proteins operates through multiple cooperative interactions, at least some of which are redundant. The physical separation of the Rap1p interaction region of Sir3p from parts of the protein required for Sir complex formation and histone binding raises the possibility that Rap1p can participate directly in the maintenance of silent chromatin through the stabilization of Sir complex-nucleosome interactions.
酿酒酵母中交配型基因座和端粒处转录沉默的起始需要将Sir2/3/4(沉默信息调节因子)蛋白复合物募集到染色体上,这至少部分是通过其与沉默子和端粒结合蛋白Rap1p的结合来实现的。Sir3p和Sir4p是沉默染色质的结构成分,它们可以自我结合、相互作用,并与组蛋白H3和H4的氨基末端尾巴结合。我们在Sir3p中鉴定出一个位于氨基酸455至481之间的小区域,该区域对于与Rap1p的羧基末端结合是必需且充分的,但对于Sir复合物的形成或组蛋白结合并非必需。缺失该区域的SIR3突变会导致HMR和端粒处的沉默缺陷。然而,这种抑制作用的损害远小于Rap1p羧基末端截短导致的Sir3p结合缺陷所表现出的损害。这种差异可能是由于Rap1p羧基末端能够独立与Sir4p相互作用,我们通过体外结合和双杂交试验证明了这一点。值得注意的是,Rap1p-Sir4p双杂交相互作用不需要Sir3p,并且通过Rap1p羧基末端的突变而被消除。我们提出,Sir3p和Sir4p都可以在交配型沉默子和端粒处直接且独立地与Rap1p结合,并表明Rap1p介导的Sir蛋白募集通过多种协同相互作用起作用,其中至少一些是冗余的。Sir3p的Rap1p相互作用区域与Sir复合物形成和组蛋白结合所需的蛋白质部分在物理上是分开的,这增加了Rap1p可以通过稳定Sir复合物-核小体相互作用直接参与沉默染色质维持的可能性。