Tsuno A, Miyoshi K, Tsujii R, Miyakawa T, Mizuta K
Department of Molecular Biotechnology, Graduate School of Advanced Sciences of Matter, Hiroshima University, Higashi-Hiroshima 739-8527, Japan.
Mol Cell Biol. 2000 Mar;20(6):2066-74. doi: 10.1128/MCB.20.6.2066-2074.2000.
A secretory defect causes specific and significant transcriptional repression of both ribosomal protein and rRNA genes (K. Mizuta and J. R. Warner, Mol. Cell. Biol. 14:2493-2502, 1994), suggesting the coupling of plasma membrane and ribosome syntheses. In order to elucidate the molecular mechanism of the signaling pathway, we isolated a cold-sensitive mutant with a mutation in a gene termed RRS1 (regulator of ribosome synthesis), which appeared to be defective in the signaling pathway. The rrs1-1 mutation greatly reduced transcriptional repression of both rRNA and ribosomal protein genes that is caused by a secretory defect. RRS1 is a novel, essential gene encoding a nuclear protein of 203 amino acid residues that is conserved in eukaryotes. A conditional rrs1-null mutant was constructed by placing RRS1 under the control of the GAL1 promoter. Rrs1p depletion caused defects in processing of pre-rRNA and assembly of ribosomal subunits.
一种分泌缺陷会导致核糖体蛋白基因和rRNA基因发生特异性且显著的转录抑制(K. 水田和J. R. 华纳,《分子与细胞生物学》14:2493 - 2502,1994年),这表明质膜合成与核糖体合成之间存在偶联关系。为了阐明该信号通路的分子机制,我们分离出了一个冷敏感突变体,其在一个名为RRS1(核糖体合成调节因子)的基因中发生了突变,该突变体在信号通路中似乎存在缺陷。rrs1 - 1突变极大地降低了由分泌缺陷引起的rRNA和核糖体蛋白基因的转录抑制。RRS1是一个新的必需基因,编码一个由203个氨基酸残基组成的核蛋白,该蛋白在真核生物中保守。通过将RRS1置于GAL1启动子的控制之下构建了一个条件性rrs1缺失突变体。Rrs1p的缺失导致前体rRNA加工和核糖体亚基组装出现缺陷。