Pu Yunting, Luo Xinjuan, Bassham Diane C
Department of Genetics, Development and Cell Biology, Iowa State University, AmesIA, United States.
Interdepartmental Genetics Program, Iowa State University, AmesIA, United States.
Front Plant Sci. 2017 Jul 11;8:1204. doi: 10.3389/fpls.2017.01204. eCollection 2017.
Autophagy is a critical process for recycling of cytoplasmic materials during environmental stress, senescence and cellular remodeling. It is upregulated under a wide range of abiotic stress conditions and is important for stress tolerance. Autophagy is repressed by the protein kinase target of rapamycin (TOR), which is activated in response to nutrients and in turn upregulates cell growth and translation and inhibits autophagy. Down-regulation of TOR in leads to constitutive autophagy and to decreased growth, but the relationship to stress conditions is unclear. Here, we assess the extent to which TOR controls autophagy activation by abiotic stress. Overexpression of inhibited autophagy activation by nutrient starvation, salt and osmotic stress, indicating that activation of autophagy under these conditions requires down-regulation of TOR activity. In contrast, TOR overexpression had no effect on autophagy induced by oxidative stress or ER stress, suggesting that activation of autophagy by these conditions is independent of TOR function. The plant hormone auxin has been shown previously to up-regulate TOR activity. To confirm the existence of two pathways for activation of autophagy, dependent on the stress conditions, auxin was added exogenously to activate TOR, and the effect on autophagy under different conditions was assessed. Consistent with the effect of TOR overexpression, the addition of the auxin NAA inhibited autophagy during nutrient deficiency, salt and osmotic stress, but not during oxidative or ER stress. NAA treatment was unable to block autophagy induced by a TOR inhibitor or by a mutation in the TOR complex component , indicating that auxin is upstream of TOR in the regulation of autophagy. We conclude that repression of auxin-regulated TOR activity is required for autophagy activation in response to a subset of abiotic stress conditions.
自噬是环境应激、衰老和细胞重塑过程中细胞质物质循环利用的关键过程。在多种非生物胁迫条件下，自噬被上调，对胁迫耐受性很重要。自噬受到雷帕霉素靶蛋白激酶（TOR）的抑制，TOR在营养物质响应下被激活，进而上调细胞生长和翻译并抑制自噬。TOR下调导致组成型自噬和生长减少，但与胁迫条件的关系尚不清楚。在这里，我们评估TOR在多大程度上通过非生物胁迫控制自噬激活。[此处原文缺失相关蛋白名称]的过表达抑制了营养饥饿、盐和渗透胁迫引起的自噬激活，表明在这些条件下自噬的激活需要TOR活性的下调。相反，TOR过表达对氧化应激或内质网应激诱导的自噬没有影响，表明这些条件下自噬的激活与TOR功能无关。植物激素生长素先前已被证明可上调TOR活性。为了证实存在两种依赖于胁迫条件的自噬激活途径，外源添加生长素以激活TOR，并评估其在不同条件下对自噬的影响。与TOR过表达的效果一致，添加生长素萘乙酸（NAA）在营养缺乏、盐和渗透胁迫期间抑制自噬，但在氧化或内质网应激期间则不然。NAA处理无法阻断TOR抑制剂或TOR复合物组分[此处原文缺失相关组分名称]突变诱导的自噬，表明生长素在自噬调节中位于TOR的上游。我们得出结论，在响应一部分非生物胁迫条件时，自噬激活需要抑制生长素调节的TOR活性。
