Over-expression of mitochondrial heat shock protein 70 suppresses programmed cell death in rice

被引：119

作者：

Qi, Yaocheng ^{[1
]}

Wang, Hongjuan ^{[1
]}

Zou, Yu ^{[1
]}

Liu, Cheng ^{[1
]}

Liu, Yanqi ^{[1
]}

Wang, Ying ^{[1
]}

Zhang, Wei ^{[1
]}

机构：

[1] Nanjing Agr Univ, Coll Life Sci, Nanjing 210095, Jiangsu, Peoples R China

来源：

FEBS LETTERS | 2011年 / 585卷 / 01期

基金：

中国国家自然科学基金;

关键词：

Mitochondrial heat shock protein 70; Mitochondrial membrane potential; Programmed cell death; Reactive oxygen species; Oryza sativa; HEAT-SHOCK; PERMEABILITY TRANSITION; STRESS; HSP70; TRANSFORMATION; PROTECTION; APOPTOSIS; PROTEASE;

D O I：

10.1016/j.febslet.2010.11.051

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

In this study, we identified and functionally characterized the mitochondrial heat shock protein 70 (mtHsp70). Over-expression of mtHsp70 suppressed heat-and H2O2-induced programmed cell death (PCD) in rice protoplasts, as reflected by higher cell viability, decreased DNA laddering and chromatin condensation. Mitochondrial membrane potential (Delta psi(m)) after heat shock was destroyed gradually in protoplasts, but mtHsp70 over-expression showed higher Delta psi(m) relative to the vector control cells, and partially inhibited cytochrome c release from mitochondria to cytosol. Heat treatment also significantly increased reactive oxygen species (ROS) generation, a phenomenon not observed in protoplasts over-expressing mtHsp70. Together, these results suggest that mtHsp70 may suppress PCD in rice protoplasts by maintaining mitochondrial Delta psi(m) and inhibiting the amplification of ROS. (C) 2010 Federation of European Biochemical Societies. Published by Elsevier B. V. All rights reserved.

引用

页码：231 / 239

页数：9

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