The mitochondrial small heat-shock protein protects NADH:ubiquinone oxidoreductase of the electron transport chain during heat stress in plants
The mitochondrial small heat-shock protein protects NADH:ubiquinone oxidoreductase of the electron transport chain during heat stress in plants
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DOI：
10.1016/s0014-5793(98)00669-3
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发表时间：
1998-07-03
期刊：
影响因子：
3.5
通讯作者：
Heckathorn, SA
中科院分区：
文献类型：
--
作者：
Downs, CA;Heckathorn, SA
使用蛋白质特异性抗体对亚线粒体囊泡中的线粒体小热休克蛋白（lmw Hsp）进行功能失活，表明该蛋白质保护NADH：泛醌氧化还原酶（复合物I），并因此保护从复合物I到细胞色素c：O（2）氧化还原酶（复合物IV）的电子传递。Lmw Hsp功能完全解释了预热胁迫植物中复合物I电子传递的热适应。此外，纯化的低分子量热休克蛋白submitochondrial囊泡缺乏这种热休克蛋白增加复合物I电子传递率100%，在submitochondrial囊泡在高温下测定。这些结果表明，线粒体Imw热休克蛋白的生产是一个重要的适应热胁迫在植物中。(C)1998年欧洲生物化学学会联合会。
Functional inactivation of the mitochondrial small heat-shock protein (lmw Hsp) in submitochondrial vesicles using protein-specific antibodies indicated that this protein protects NADH:ubiquinone oxidoreductase (complex I), and consequently electron transport from complex I to cytochrome c:O(2) oxidoreductase (complex IV). Lmw Hsp function completely accounted for heat acclimation of complex I electron transport in pre-heat-stressed plants. Addition of purified lmw Hsp to submitochondrial vesicles lacking this Hsp increased complex I electron transport rates 100% in submitochondrial vesicles assayed at high temperatures. These results indicate that production of the mitochondrial Imw Hsp is an important adaptation to heat stress in plants. (C) 1998 Federation of European Biochemical Societies.