酵母线粒体核糖体蛋白Rml2p突变与过氧化氢酶基因表达缺陷相关

Ruth A. Hagerman , Pamela J. Trotter
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引用次数: 9

摘要

酵母菌株含有一个新的温度敏感的RML2基因等位基因,编码线粒体核糖体大亚基的一个组成部分,在醋酸盐上生长正常,在甘油上生长缓慢,在油酸上不能生长。这些细胞,标记为rm2 (fat21),明显无法诱导过氧化物酶体功能,这可以通过油酸诱导β -氧化的缺乏来证明。然而,油酸对编码过氧化物酶体-氧化核心酶的基因的调控是正常的。相反,CTA1(过氧化氢酶)mRNA表达和酶活性的上调被中断。通过比较过氧化氢酶和β -氧化基因的诱导需求,我们假设rml2(fat21)突变改变了转录因子Adr1p的活性。为了支持这一假设,ADR1在rml2(fat21)细胞中的过表达可以恢复CTA1的诱导。对rml2(fat21)菌株线粒体的几项测定表明线粒体功能正常。因此,adr1p相关基因调控的调节不是由于明显的线粒体功能障碍。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
A Mutation in the Yeast Mitochondrial Ribosomal Protein Rml2p Is Associated with a Defect in Catalase Gene Expression

Yeast strains containing a new temperature-sensitive allele of the RML2 gene, encoding a component of the large subunit of the mitochondrial ribosome, display normal growth on acetate, slowed growth on glycerol and an inability to grow on oleic acid. These cells, denoted rml2(fat21), have an apparent inability to induce peroxisomal function, as evidenced by a deficiency in oleic acid induction of beta-oxidation. However, the oleic acid regulation of genes encoding core enzymes of peroxisomal beta-oxidation is normal. In contrast, up-regulation of CTA1 (catalase) mRNA expression and enzyme activity is interrupted. Upon comparison of the induction requirements of catalase and the genes of beta-oxidation, we hypothesized that the rml2(fat21) mutation alters the activity of the transcription factor Adr1p. In support of this hypothesis, over-expression of ADR1 in rml2(fat21) cells restores CTA1 induction. Several assays of mitochondria from rml2(fat21) strains suggest normal mitochondrial function. Thus, the modulation of Adr1p-associated gene regulation is not due to overt mitochondrial dysfunction.

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