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热休克蛋白HSP60可缓解线粒体RNA缺陷型温度敏感型mna2 pet突变体的表型。

Heat shock protein HSP60 can alleviate the phenotype of mitochondrial RNA-deficient temperature-sensitive mna2 pet mutants.

作者信息

Sanyal A, Harington A, Herbert C J, Groudinsky O, Slonimski P P, Tung B, Getz G S

机构信息

Department of Medicine, University of Chicago, IL 60637.

出版信息

Mol Gen Genet. 1995 Jan 6;246(1):56-64. doi: 10.1007/BF00290133.

Abstract

mna2, which belongs to the class I temperature-sensitive pet mutants that lose mitochondrial (mt)RNA at restrictive temperature, was shown by complementation and sequence determination to correspond to the gene coding for HSP60. Both mna2-1 and mna2-2, the two available alleles of mna2, have conservative single amino acid substitutions in the HSP60 gene. Valine substitutes for an alanine (position 47) in mna2-1, and an isoleucine substitutes for a valine (position 77) in mna2-2. These substitutions result in defects in respiration and in steady-state mtRNA accumulation. Wild-type hsp60 alleviates the mtRNA phenotype completely, while partially relieving the respiratory deficiency.

摘要

mna2属于I类温度敏感型pet突变体,在限制温度下会丢失线粒体(mt)RNA,通过互补和序列测定表明它对应于编码HSP60的基因。mna2的两个可用等位基因mna2-1和mna2-2在HSP60基因中都有保守的单氨基酸替换。在mna2-1中缬氨酸替代了丙氨酸(第47位),在mna2-2中异亮氨酸替代了缬氨酸(第77位)。这些替换导致呼吸作用和稳态mtRNA积累出现缺陷。野生型hsp60能完全缓解mtRNA表型,同时部分缓解呼吸缺陷。

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