Temperature-sensitive mutations in the Saccharomyces cerevisiae MRT4, GRC5, SLA2 and THS1 genes result in defects in mRNA turnover.
Temperature-sensitive mutations in the Saccharomyces cerevisiae MRT4, GRC5, SLA2 and THS1 genes result in defects in mRNA turnover.
复制标题
酿酒酵母 MRT4、GRC5、SLA2 和 THS1 基因中的温度敏感突变会导致 mRNA 周转缺陷。
DOI：
10.1093/genetics/153.1.35
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发表时间：
1999
期刊：
影响因子：
3.3
通讯作者：
Jacobson,A
中科院分区：
文献类型：
--
作者：
Zuk,D;Belk,JP;Jacobson,A
在对涉及mRNA周转的因素的筛选中，四个对温度敏感的酵母菌株(ts1189、ts942、ts817和ts1100)在几个mRNAs的衰变中显示出缺陷。生长和mRNA衰退缺陷的互补以及遗传实验表明，ts1189突变于先前未知的MRT4基因，ts942突变于GRC5(编码L9核糖体蛋白)，ts817包含SLA2突变(编码膜蛋白)，ts1100包含THS1突变(编码苏氨酰-tRNA合成酶)。四个突变体中的三个(mrt4、grc5和slA2)在蛋白质合成方面没有缺陷，这表明这些菌株含有可能在mRNA衰退中发挥特殊作用的因子的突变。然而，在ths1株中观察到的mRNA稳定可能是由于在37°时观察到该突变体的翻译显著下降。虽然这三个有趣的突变体似乎编码了新的信使核糖核酸衰变因子，但至少有一个可能与先前描述的信使核糖核酸衰变途径有关。NMD3基因的过表达抑制了ts942(Grc5)细胞的生长和mRNA衰退缺陷，该基因编码的蛋白与无义介导的衰退蛋白Upf1p参与了双杂交相互作用。
In a screen for factors involved in mRNA turnover, four temperature-sensitive yeast strains (ts1189, ts942, ts817, and ts1100) exhibited defects in the decay of several mRNAs. Complementation of the growth and mRNA decay defects, and genetic experiments, revealed that ts1189 is mutated in the previously unknown MRT4 gene, ts942 is mutated in GRC5 (encoding the L9 ribosomal protein), ts817 contains a mutation in SLA2 (encoding a membrane protein), and ts1100 contains a mutation in THS1 (encoding the threonyl-tRNA synthetase). Three of the four mutants (mrt4, grc5, and sla2) were not defective in protein synthesis, suggesting that these strains contain mutations in factors that may play a specific role in mRNA decay. The mRNA stabilization observed in the ths1 strain, however, could be due to the significant drop in translation observed in this mutant at 37°. While the three interesting mutants appear to encode novel mRNA decay factors, at least one could be linked to a previously characterized mRNA decay pathway. The growth and mRNA decay defects of ts942 (grc5) cells were suppressed by overexpression of the NMD3 gene, encoding a protein shown to participate in a two-hybrid interaction with the nonsense-mediated decay protein Upf1p.