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首页> 外文期刊>Molecular and Cellular Biology >The Saccharomyces cerevisiae Hyperrecombination Mutanthpr1Δ Is Synthetically Lethal with Two Conditional Alleles of the Acetyl Coenzyme A Carboxylase Gene and Causes a Defect in Nuclear Export of Polyadenylated RNA
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The Saccharomyces cerevisiae Hyperrecombination Mutanthpr1Δ Is Synthetically Lethal with Two Conditional Alleles of the Acetyl Coenzyme A Carboxylase Gene and Causes a Defect in Nuclear Export of Polyadenylated RNA

机译：酿酒酵母超重组Mutanthpr1Δ与两个条件的乙酰辅酶A羧化酶基因等位基因合成致死，并导致聚腺苷酸化RNA的核出口缺陷。

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In a screen for mutants that display synthetic lethal interaction with hpr1Δ, a hyperrecombination mutant ofSaccharomyces cerevisiae, we have isolated a novel cold-sensitive allele of the acetyl coenzyme A (CoA) carboxylase gene,acc1cs , encoding the rate-limiting enzyme of fatty acid synthesis. The synthetic lethal phenotype of theacc1cs hpr1Δ double mutant was only partially complemented by exogenous fatty acids. hpr1Δ was also synthetically lethal with a previously isolated, temperature-sensitive allele of ACC1, mtr7 (mRNA transport), indicating that the lethality of the acc1cshpr1Δ double mutant was not allele specific. The basis for the interaction between conditional acc1 alleles andhpr1Δ was investigated in more detail. In thehpr1Δ mutant background, acetyl-CoA carboxylase enzyme activity was reduced about 15-fold and steady-state levels of biotinylated Acc1p and ACC1 mRNA were reduced 2-fold. The reduced Acc1p activity in hpr1Δ cells, however, did not result in an altered lipid or fatty acid composition of the mutant membranes but rendered cells hypersensitive to soraphen A, an inhibitor of Acc1p. Similar to mtr7, hpr1Δ andacc1cs mutant cells displayed a defect in nuclear export of polyadenylated RNA. Oversized transcripts were detected in hpr1Δ, and rRNA processing was disturbed, but pre-mRNA splicing appeared wild type. Surprisingly, the transport defect of hpr1Δ and acc1cs mutant cells was accompanied by an altered ring-shaped structure of the nucleolus. These observations suggest that the basis for the synthetic lethal interaction between hpr1Δ and acc1 may lie in a functional overlap of the two mutations in nuclear poly(A)+ RNA production and export that results in an altered structure of the nucleolus.
机译：在筛选中显示与 hpr1 Δ（酿酒酵母（Saccharomyces cerevisiae）的超重组突变体的超重组突变体）发生合成致死相互作用的突变体中，我们分离出了乙酰辅酶A（A CoA）羧化酶基因， acc1 cs ，编码脂肪酸合成的限速酶。 acc1 cs hpr1 Δ双突变体的合成致死表型仅部分被外源脂肪酸所补充。 hpr1 Δ也与先前分离的，对温度敏感的等位基因 ACC1 ， mtr7 （mRNA转运）具有合成杀伤力，这表明 acc1 cs hpr1 Δ双突变体不是等位基因特异性的。进一步研究了条件 acc1 等位基因与 hpr1 Δ之间相互作用的基础。在 hpr1 Δ突变体背景下，乙酰辅酶A羧化酶活性降低了约15倍，而生物素化的Acc1p和 ACC1 mRNA的稳态水平降低了2倍。然而， hpr1 Δ细胞中Acc1p活性的降低并未导致突变膜的脂质或脂肪酸组成发生变化，但使细胞对Acc1p抑制剂soraphen A过敏。与 mtr7 类似， hpr1 Δ和 acc1 cs 突变细胞在聚腺苷酸化RNA的核输出中显示出缺陷。在 hpr1 Δ中检测到过大的转录本，干扰了rRNA的加工，但mRNA之前的剪接显示为野生型。令人惊讶的是， hpr1 Δ和 acc1 cs 突变细胞的运输缺陷伴随着核仁环状结构的改变。这些观察结果表明， hpr1 Δ和 acc1 之间合成致死相互作用的基础可能在于核poly（A） +中两个突变的功能重叠。 RNA的产生和输出导致核仁结构发生改变。

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