近日，中科院植物研究所田世平研究员领导的课题组通过蛋白质组学结合免疫杂交以及细胞生物学等技术解析了线粒体蛋白氧化损伤调控果实成熟衰老的可能机制。该成果发表在Journal of Proteome Research（2009, 8: 2449-2462）杂志上。
果实为开花植物特有的发育器官，在种子成熟和传播过程中发挥着重要作用，肉质果实也是人们饮食的重要组成部分。成熟衰老是果实的重要特征之一，解析果实成熟衰老的机制有着重要的理论和应用价值。根据“衰老的线粒体学说”，线粒体在细胞衰老过程中发挥着重要作用，但是其具体机理并不清楚，线粒体与植物衰老的关系更是鲜有报道。研究人员从活性氧代谢的角度，通过蛋白质组学、蛋白免疫杂交以及其他生理生化分析，揭示了线粒体蛋白氧化损伤与果实成熟衰老的关系。研究发现包括线粒体外膜蛋白、三羧酸循环相关蛋白以及抗氧化酶在内的线粒体蛋白在果实正常成熟衰老过程中发生了不同程度的氧化损伤。通过加速果实衰老和延缓衰老的方式，研究人员进一步从正反两个方面开展了工作，并认为这些蛋白在果实成熟衰老过程中可能发挥着重要作用。
该研究成果中所涉及的果实线粒体提取纯化、线粒体蛋白双向电泳，以及蛋白质氧化损伤等技术将为进一步解析线粒体在果实成熟衰老过程中的重要作用提供重要的技术平台。（生物谷Bioon.com）
生物谷推荐原始出处：
J. Proteome Res., 2009, 8 (5), pp 2449–2462 DOI: 10.1021/pr801046m
Oxidative Damage of Mitochondrial Proteins Contributes to Fruit Senescence: A Redox Proteomics Analysis
Guozheng Qin?, Xianghong Meng?, Qing Wang and Shiping Tian*
Key Laboratory of Photosynthesis and Environmental Molecular Physiology, Institute of Botany, Chinese Academy of Sciences, Beijing 100093, China
Oxidative damage to mitochondria caused by reactive oxygen species (ROS) has been implicated in the process of senescence as well as a number of senescence-related disorders in a variety of organisms. Whereas mitochondrial DNA was shown to be oxidatively modified during cellular senescence, mitochondrial protein oxidation is not well-understood. With the use of high-resolution, two-dimensional gel electrophoresis coupled with immunoblotting, we show here that protein carbonylation, a widely used marker of protein oxidation, increased in mitochondria during the senescence of peach fruit. Specific mitochondrial proteins including outer membrane transporter (voltage-dependent anion-selective channel, VDAC), tricarboxylic acid cycle enzymes (malate dehydrogenase and aconitase), and antioxidant proteins (manganese superoxide dismutase, MnSOD) were found as the targets. The oxidative modification was concomitant with a change of VDAC function and loss of catalytic activity of malate dehydrogenase and MnSOD, which in turn facilitated the release of superoxide radicals in mitochondria. Reduction of ROS content by lowering the environmental temperature prevented the accumulation of protein carbonylation in mitochondria and retarded fruit senescence, whereas treatment of fruit with H2O2 had the opposite effect. Our data suggest that oxidative damage of specific mitochondrial proteins may be responsible for impairment of mitochondrial function, thus, leading to fruit senescence. Proteomics analysis of mitochondrial redox proteins provides considerable information on the molecular mechanisms involved in the progression of fruit senescence.
