Genome-wide responses to mitochondrial dysfunction
Genome-wide responses to mitochondrial dysfunction
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DOI：
10.1091/mbc.12.2.297
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发表时间：
2001-02-01
影响因子：
3.3
通讯作者：
Butow, RA
中科院分区：
文献类型：
--
作者：
Epstein, CB;Waddle, JA;Butow, RA
线粒体功能障碍可导致不同的细胞和生物体反应。我们使用DNA微阵列来表征酿酒酵母中不同线粒体扰动的转录反应。我们研究了氧化磷酸化抑制剂抗霉素，羰基氰间氯苯腙，或寡霉素处理的氧化缺陷的小细胞和氧化能力的野生型细胞。我们发现，呼吸功能障碍，但不抑制线粒体ATP合成本身，诱导一套基因与过氧化物酶体的活动和代谢恢复（回补）途径，这将减轻损失的一个完整的三羧酸循环。阵列的数据表明，直接显微镜观察细胞表达的衍生物的绿色荧光蛋白与过氧化物酶体基质靶向信号证实，呼吸不足显着诱导过氧化物酶体生物合成。携带RTG1、RTG2或RTG3无效等位基因的细胞的转录谱分析表明，酵母中这些细胞器之间存在多种串扰途径。
Mitochondrial dysfunction can lead to diverse cellular and organismal responses. We used DNA microarrays to characterize the transcriptional responses to different mitochondrial perturbations in Saccharomyces cerevisiae. We examined respiratory-deficient petite cells and respiratory-competent wild-type cells treated with the inhibitors of oxidative phosphorylation antimycin, carbonyl cyanide m-chlorophenylhydrazone, or oligomycin. We show that respiratory deficiency, but not inhibition of mitochondrial ATP synthesis per se, induces a suite of genes associated with both peroxisomal activities and metabolite-restoration (anaplerotic) pathways that would mitigate the loss of a complete tricarboxylic acid cycle. The array data suggested, and direct microscopic observation of cells expressing a derivative of green fluorescent protein with a peroxisomal matrix-targeting signal confirmed, that respiratory deficiency dramatically induces peroxisome biogenesis. Transcript profiling of cells harboring null alleles of RTG1, RTG2, or RTG3, genes known to control signaling from mitochondria to the nucleus, suggests that there are multiple pathways of cross-talk between these organelles in yeast.