Department of Molecular Genetics and Program in Molecular, Cellular and Developmental Biology, The Ohio State University, Columbus, OH, USA.
Autophagy. 2010 Feb;6(2):294-5. doi: 10.4161/auto.6.2.11129. Epub 2010 Feb 6.
Macroautophagy (hereafter autophagy) is a conserved membrane trafficking pathway responsible for the turnover of cytosolic protein and organelles during periods of nutrient deprivation. This pathway is also linked to a number of processes important for human health, including tumor suppression, innate immunity and the clearance of protein aggregates. As a result, there is tremendous interest in autophagy as a potential point of therapeutic intervention in a variety of pathological states. To achieve this goal, it is imperative that we develop a thorough understanding of the normal regulation of this process in eukaryotic cells. The Tor protein kinases clearly constitute a key element of this control as Tor activity inhibits this degradative process in all organisms examined, from yeast to man. Here, we discuss recent work indicating that the cAMP-dependent protein kinase (PKA) also plays a critical role in controlling autophagy in the budding yeast, Saccharomyces cerevisiae. A model describing how PKA activity might influence this degradative process, and how this control might be integrated with that of the Tor pathway, is presented.
自噬作用（以下简称自噬）是一种保守的膜运输途径，负责在营养缺乏时期细胞溶质蛋白和细胞器的周转。这条途径还与许多对人类健康很重要的过程有关，包括肿瘤抑制、先天免疫和蛋白质聚集体的清除。因此，自噬作为治疗各种病理状态的潜在靶点，引起了极大的关注。为了实现这一目标，我们必须深入了解真核细胞中这一过程的正常调控。Tor 蛋白激酶显然是这种控制的关键因素，因为 Tor 的活性抑制了从酵母到人等所有被检查的生物体中的这个降解过程。在这里，我们讨论了最近的工作，表明 cAMP 依赖性蛋白激酶（PKA）也在控制芽殖酵母酿酒酵母中的自噬中发挥关键作用。提出了一个描述 PKA 活性如何影响这个降解过程，以及这种控制如何与 Tor 途径的控制相整合的模型。
