近日,，中科院植物研究所田世平研究員領(lǐng)導的課題組通過蛋白質(zhì)組學結(jié)合免疫雜交以及細胞生物學等技術(shù)解析了線粒體蛋白氧化損傷調(diào)控果實成熟衰老的可能機制,。該成果發(fā)表在Journal of Proteome Research（2009, 8: 2449-2462）雜志上,。
果實為開花植物特有的發(fā)育器官,，在種子成熟和傳播過程中發(fā)揮著重要作用,，肉質(zhì)果實也是人們飲食的重要組成部分,。成熟衰老是果實的重要特征之一,，解析果實成熟衰老的機制有著重要的理論和應用價值,。根據(jù)“衰老的線粒體學說”,，線粒體在細胞衰老過程中發(fā)揮著重要作用，但是其具體機理并不清楚,，線粒體與植物衰老的關(guān)系更是鮮有報道,。研究人員從活性氧代謝的角度，通過蛋白質(zhì)組學,、蛋白免疫雜交以及其他生理生化分析,，揭示了線粒體蛋白氧化損傷與果實成熟衰老的關(guān)系。研究發(fā)現(xiàn)包括線粒體外膜蛋白,、三羧酸循環(huán)相關(guān)蛋白以及抗氧化酶在內(nèi)的線粒體蛋白在果實正常成熟衰老過程中發(fā)生了不同程度的氧化損傷,。通過加速果實衰老和延緩衰老的方式，研究人員進一步從正反兩個方面開展了工作,，并認為這些蛋白在果實成熟衰老過程中可能發(fā)揮著重要作用,。
該研究成果中所涉及的果實線粒體提取純化、線粒體蛋白雙向電泳,，以及蛋白質(zhì)氧化損傷等技術(shù)將為進一步解析線粒體在果實成熟衰老過程中的重要作用提供重要的技術(shù)平臺,。（生物谷Bioon.com）
生物谷推薦原始出處：
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.
