The cold sensitivity of a mutant of Saccharomyces cerevisiae lacking a mitochondrial heat shock protein 70 is suppressed by loss of mitochondrial DNA.
The cold sensitivity of a mutant of Saccharomyces cerevisiae lacking a mitochondrial heat shock protein 70 is suppressed by loss of mitochondrial DNA.
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DOI：
10.1083/jcb.134.3.603
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发表时间：
1996-08
期刊：
影响因子：
--
通讯作者：
Craig E
中科院分区：
文献类型：
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作者：
Schilke B;Forster J;Davis J;James P;Walter W;Laloraya S;Johnson J;Miao B;Craig E
SSH1是一个新发现的芽殖酵母酿酒酵母热休克蛋白（hsp70）多基因家族的成员，编码一种定位于线粒体基质的蛋白。SSH1基因的缺失导致在23摄氏度或30摄氏度下生长极其缓慢，但在37摄氏度下几乎是野生型生长。线粒体的基质含有另一种热休克蛋白70，Ssc 1，它是生长所必需的，也是蛋白质转运到线粒体中所必需的。与SSC 1突变体不同，SSH1突变体与野生型相比，在从胞质溶胶向基质输入几种蛋白质方面没有表现出可检测的缺陷。Ssc 1表达的增加部分抑制了SSH 1突变体的冷敏感性生长缺陷，表明当以增加的量存在时，Ssc 1可以至少部分地执行Ssh 1的正常功能。自发抑制的SSH1无效突变体的冷敏感表型，在23摄氏度的高频率获得，都被发现是呼吸缺陷。在分析的16个抑制子中，有15个缺乏线粒体DNA，而第16个数量减少。我们认为，Ssh1是正常的线粒体DNA复制所必需的，并且在Ssh1细胞中破坏这一过程会导致在低温下线粒体功能的缺陷。
SSH1, a newly identified member of the heat shock protein (hsp70) multigene family of the budding yeast Saccharomyces cerevisiae, encodes a protein localized to the mitochondrial matrix. Deletion of the SSH1 gene results in extremely slow growth at 23 degrees C or 30 degrees C, but nearly wild-type growth at 37 degrees C. The matrix of the mitochondria contains another hsp70, Ssc1, which is essential for growth and required for translocation of proteins into mitochondria. Unlike SSC1 mutants, an SSH1 mutant showed no detectable defects in import of several proteins from the cytosol to the matrix compared to wild type. Increased expression of Ssc1 partially suppressed the cold- sensitive growth defect of the SSH1 mutant, suggesting that when present in increased amounts, Ssc1 can at least partially carry out the normal functions of Ssh1. Spontaneous suppressors of the cold-sensitive phenotype of an SSH1 null mutant were obtained at a high frequency at 23 degrees C, and were all found to be respiration deficient. 15 of 16 suppressors that were analyzed lacked mitochondrial DNA, while the 16th had reduced amounts. We suggest that Ssh1 is required for normal mitochondrial DNA replication, and that disruption of this process in ssh1 cells results in a defect in mitochondrial function at low temperatures.