Laurenson P, Rine J
Department of Molecular and Cellular Biology, University of California, Berkeley 94720.
Genetics. 1991 Nov;129(3):685-96. doi: 10.1093/genetics/129.3.685.
The repression of transcription of the silent mating-type locus HMRa in the yeast Saccharomyces cerevisiae requires the four SIR proteins, histone H4 and a flanking site designated HMR-E. The SUM1-1 mutation alleviated the need for many of these components in transcriptional repression. In the absence of each of the SIR proteins, SUM1-1 restored repression in MAT alpha strains; thus, SUM1-1 appeared to bypass the need for the SIR genes in repression of HMRa. Repression was not specific to the genes normally present at HMR, since the TRP1 gene placed at HMR was repressed by SUM1-1 in a sir3 strain. Therefore, like the mechanisms of silencing normally used at HMR, silencing by SUM1-1 was gene-nonspecific. SUM1-1 suppressed point mutations in histone H4, but failed to suppress strongly a deletion mutation in histone H4. Similarly, SUM1-1 suppressed mutations in the three known elements of HMR-E, but was unable to suppress a deletion of HMR-E. These epistasis analyses implied that the functions required for repression at HMR can be ordered, with the SIR genes and silencer elements acting upstream of SUM1-1. SUM1-1 itself may function at the level of chromatin in the assembly of inactive DNA at the silent mating-type loci.
在酿酒酵母中,沉默交配型基因座HMRa的转录抑制需要四种SIR蛋白、组蛋白H4以及一个名为HMR-E的侧翼位点。SUM1-1突变减轻了转录抑制中对许多这些组分的需求。在缺乏每种SIR蛋白的情况下,SUM1-1在MATα菌株中恢复了抑制作用;因此,SUM1-1似乎在HMRa的抑制中绕过了对SIR基因的需求。抑制并非HMR中正常存在的基因所特有的,因为置于HMR的TRP1基因在sir3菌株中被SUM1-1抑制。因此,与HMR中正常使用的沉默机制一样,SUM1-1介导的沉默是非基因特异性的。SUM1-1抑制了组蛋白H4中的点突变,但未能强烈抑制组蛋白H4中的缺失突变。同样,SUM1-1抑制了HMR-E的三个已知元件中的突变,但无法抑制HMR-E的缺失。这些上位性分析表明,HMR抑制所需的功能可以排序,SIR基因和沉默子元件在SUM1-1的上游起作用。SUM1-1本身可能在沉默交配型基因座上无活性DNA组装的染色质水平发挥作用。