Stettler S, Chiannilkulchai N, Hermann-Le Denmat S, Lalo D, Lacroute F, Sentenac A, Thuriaux P
Département de Biologie Cellulaire et Moléculaire, C.E.A. Centre d'Etudes de Saclay, Gif sur Yvette, France.
Mol Gen Genet. 1993 May;239(1-2):169-76. doi: 10.1007/BF00281615.
A multicopy genomic library of Saccharomyces cerevisiae (strain FL100) was screened for its ability to suppress conditionally defective mutations altering the 31 kDa subunit (rpc31-236) or the 53 kDa subunit (rpc53-254/424) of RNA polymerase III. In addition to allele-specific suppressors, we identified seven suppressor clones that acted on both mutations and also suppressed several other conditional mutations defective in RNA polymerases I or II. All these clones harbored a complete copy of the SSD1 gene. The same pleiotropic suppression pattern was found with the dominant SSD1-v allele present in some laboratory strains of S. cerevisiae. SSD1-v was previously shown to suppress mutations defective in the SIT4 gene product (a predicted protein phosphatase subunit) or in the regulatory subunit of the cyclic AMP-dependent protein kinase. We propose that the SSD1 gene product modulates the activity (or the level) of the three nuclear RNA polymerases, possibly by altering their degree of phosphorylation.
对酿酒酵母（菌株FL100）的多拷贝基因组文库进行筛选，以检测其抑制条件性缺陷突变的能力，这些突变改变了RNA聚合酶III的31 kDa亚基（rpc31 - 236）或53 kDa亚基（rpc53 - 254/424）。除了等位基因特异性抑制子外，我们还鉴定出七个抑制子克隆，它们对这两种突变均起作用，并且还抑制了RNA聚合酶I或II中的其他几个条件性突变。所有这些克隆都含有SSD1基因的完整拷贝。在酿酒酵母的一些实验室菌株中存在的显性SSD1 - v等位基因也发现了相同的多效性抑制模式。之前已证明SSD1 - v可抑制SIT4基因产物（一种预测的蛋白磷酸酶亚基）或环磷酸腺苷依赖性蛋白激酶调节亚基中的缺陷突变。我们提出，SSD1基因产物可能通过改变三种核RNA聚合酶的磷酸化程度来调节其活性（或水平）。
