首页> 外文期刊>The Journal of Biochemistry >Genetic interactions of ribosome maturation factors Yvh1 and Mrt4 influence mRNA decay, glycogen accumulation, and the expression of early meiotic genes in Saccharomyces cerevisiae.
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Genetic interactions of ribosome maturation factors Yvh1 and Mrt4 influence mRNA decay, glycogen accumulation, and the expression of early meiotic genes in Saccharomyces cerevisiae.

机译:核糖体成熟因子Yvh1和Mrt4的遗传相互作用影响酿酒酵母中的mRNA衰减,糖原积累和早期减数分裂基因的表达。

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摘要

The Saccharomyces cerevisiae Yvh1, a dual-specificity protein phosphatase involved in glycogen accumulation and sporulation, is required for normal vegetative growth. To further elucidate the role of Yvh1, we generated dominant mutants suppressing the slow growth caused by YVH1 disruption. One of the mutant alleles, designated as SVH1-1 (suppressor of Deltayvh1 deletion), was identical to MRT4 (mRNA turnover) that contained a single-base substitution causing an amino acid change from Gly(68) to Asp. Mrt4(G68D) restored the deficiencies in growth and rRNA biogenesis that occurs in absence of Yvh1. Here, we report that the interaction between Mrt4 and Yvh1 is also essential for normal glycogen accumulation and mRNA decay as well as the induction of sporulation genes IME2, SPO13 and HOP1. The Mrt4(G68D) could restore the plethora of phenotypes we observed in absence of Yvh1. We found that Yvh1 is not essential for wild-type induction of the transcriptional regulator of these genes, IME1, suggesting that either translation or post-translational modification to activate Ime1 has been compromised. Since a defect in ribosome biogenesis in general can be related to other various defects, the ribosome biogenesis defect caused by absence of Yvh1 might be an indirect cause of observed phenotypes.
机译:正常营养生长需要酿酒酵母Yvh1,它是一种参与糖原积累和孢子形成的双重特异性蛋白质磷酸酶。为了进一步阐明Yvh1的作用,我们产生了抑制YVH1破坏引起的缓慢生长的显性突变体。突变等位基因之一,命名为SVH1-1(Deltayvh1缺失的抑制子),与MRT4(mRNA周转)相同,后者含有单碱基取代,导致氨基酸从Gly(68)变为Asp。 Mrt4(G68D)恢复了缺乏Yvh1时生长和rRNA生物发生的缺陷。在这里,我们报告Mrt4和Yvh1之间的相互作用对于正常糖原积累和mRNA衰变以及诱导孢子形成基因IME2,SPO13和HOP1也是必不可少的。在没有Yvh1的情况下,Mrt4(G68D)可以恢复过多的表型。我们发现,Yvh1对于这些基因IME1的转录调节因子的野生型诱导不是必需的,这表明激活Ime1的翻译或翻译后修饰已受到损害。由于核糖体生物发生的缺陷通常可以与其他各种缺陷相关,因此,由于缺乏Yvh1而引起的核糖体生物发生的缺陷可能是观察到的表型的间接原因。

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