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COXIV and SIRT2‐mediated G6PD deacetylation modulate ROS homeostasis to extend pupal lifespan
The FEBS Journal ( IF 5.5 ) Pub Date : 2020-10-15 , DOI: 10.1111/febs.15592 Shao-Lei Geng 1 , Xiao-Shuai Zhang 1 , Wei-Hua Xu 1
The FEBS Journal ( IF 5.5 ) Pub Date : 2020-10-15 , DOI: 10.1111/febs.15592 Shao-Lei Geng 1 , Xiao-Shuai Zhang 1 , Wei-Hua Xu 1
Affiliation
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Previous studies have shown that high physiological levels of reactive oxygen species (ROS) in the brain promote pupal diapause, which extends the pupal lifespan. However, the molecular mechanisms of ROS generation are unclear. In this paper, we found that mitochondrial ROS (mtROS) levels in the brains of Helicoverpa armigera diapause‐destined pupae (DP) were higher and that the expression of cytochrome oxidase subunit IV (COXIV) was lower than in NP. In addition, downregulating COXIV caused mitochondrial dysfunction which elevated mtROS levels. Protein kinase A (PKA) was downregulated in DP, which led to the downregulated expression of the mitochondrial transcription factor TFAM. Low TFAM activity failed to promote COXIV expression and resulted in the high ROS levels that induced diapause. In addition, low sirtuin 2 expression suppressed glucose‐6‐phosphate dehydrogenase (G6PD) deacetylation at K382, which led to reduced G6PD activity and low NADPH levels, thereby maintaining high levels of ROS. Two proteins, COXIV and G6PD, thus play key roles in the elevated accumulation of ROS that induce diapause and extend the pupal lifespan.
中文翻译：
COXIV和SIRT2介导的G6PD脱乙酰基调节ROS稳态以延长p的寿命
先前的研究表明，大脑中高生理水平的活性氧（ROS）会促进小儿滞育，延长小儿的寿命。但是，ROS产生的分子机制尚不清楚。在本文中，我们发现棉铃虫大脑中的线粒体ROS（mtROS）水平滞育性p（DP）高于NP，而细胞色素氧化酶亚基IV（COXIV）的表达低于NP。此外，下调COXIV会导致线粒体功能障碍，从而增加mtROS水平。蛋白激酶A（PKA）在DP中下调，这导致线粒体转录因子TFAM的表达下调。较低的TFAM活性不能促进COXIV表达，并导致高ROS水平导致滞育。此外，低sirtuin 2表达抑制了K382处的葡萄糖-6-磷酸脱氢酶（G6PD）脱乙酰基作用，从而导致G6PD活性降低和NADPH水平降低，从而保持了高水平的ROS。因此，两种蛋白质，COXIV和G6PD，在ROS升高累积中起关键作用，ROS引起滞育并延长the的寿命。
更新日期：2020-10-15
中文翻译：
COXIV和SIRT2介导的G6PD脱乙酰基调节ROS稳态以延长p的寿命
先前的研究表明，大脑中高生理水平的活性氧（ROS）会促进小儿滞育，延长小儿的寿命。但是，ROS产生的分子机制尚不清楚。在本文中，我们发现棉铃虫大脑中的线粒体ROS（mtROS）水平滞育性p（DP）高于NP，而细胞色素氧化酶亚基IV（COXIV）的表达低于NP。此外，下调COXIV会导致线粒体功能障碍，从而增加mtROS水平。蛋白激酶A（PKA）在DP中下调，这导致线粒体转录因子TFAM的表达下调。较低的TFAM活性不能促进COXIV表达，并导致高ROS水平导致滞育。此外，低sirtuin 2表达抑制了K382处的葡萄糖-6-磷酸脱氢酶（G6PD）脱乙酰基作用，从而导致G6PD活性降低和NADPH水平降低，从而保持了高水平的ROS。因此，两种蛋白质，COXIV和G6PD，在ROS升高累积中起关键作用，ROS引起滞育并延长the的寿命。
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