Overexpression of the alternative oxidase restores senescence and fertility in a long‐lived respiration‐deficient mutant of Podospora anserina
Overexpression of the alternative oxidase restores senescence and fertility in a long‐lived respiration‐deficient mutant of Podospora anserina
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DOI：
10.1046/j.1365-2958.2001.02690.x
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发表时间：
2001-12
影响因子：
3.6
通讯作者：
S. Lorin;E. Dufour;J. Boulay;O. Begel;S. Marsy;A. Sainsard-Chanet
中科院分区：
文献类型：
--
作者：
S. Lorin;E. Dufour;J. Boulay;O. Begel;S. Marsy;A. Sainsard-Chanet
一些证据表明，活性氧（ROS）在各种退行性疾病的发病机制和生物体衰老。此外，最近已经表明，植物中存在的替代途径呼吸降低了ROS线粒体的产生。另一种氧化酶（AOXp）也存在于丝状真菌鹅柄孢菌中。我们在这里表明，这种氧化酶的过度表达不会减少ROS的产生，对这种真菌的寿命，线粒体稳定性或衰老没有影响。同样，基因的失活对这些参数没有影响。相反，在细胞色素c氧化酶缺陷的长寿cox 5：：BLE突变体中替代氧化酶的过表达显著增加了突变体的ROS产生。它拯救缓慢的生长速度和女性不育，表明提高了能量水平。这种过表达也恢复衰老和线粒体DNA的不稳定性，表明这些参数是由能量水平控制，而不是由替代氧化酶的表达水平。我们还认为，这种氧化酶在生物体中的表达，自然缺乏它可以挽救呼吸系统的缺陷造成的细胞色素途径功能障碍。
Several lines of evidence have implicated reactive oxygen species (ROS) in the pathogenesis of various degenerative diseases and in organismal ageing. Furthermore, it has been shown recently that the alternative pathway respiration present in plants lowers ROS mitochondrial production. An alternative oxidase (AOXp) also occurs in the filamentous fungus Podospora anserina. We show here that overexpression of this oxidase does not decrease ROS production and has no effect on longevity, mitochondrial stability or ageing in this fungus. In the same way, inactivation of the gene has no effect on these parameters. In contrast, overexpression of the alternative oxidase in the long‐lived cox5::BLE mutant, deficient in cytochrome c oxidase, considerably increases ROS production of the mutant. It rescues slow growth rate and female sterility, indicating an improved energy level. This overexpression also restores senescence and mitochondrial DNA instability, demonstrating that these parameters are controlled by the energy level and not by the expression level of the alternative oxidase. We also suggest that expression of this oxidase in organisms naturally devoid of it could rescue respiratory defects resulting from cytochrome pathway dysfunctions.