Life Sciences Institute, and the Department of Molecular, Cellular and Developmental Biology, University of Michigan, Ann Arbor, MI 48109, United States.
Life Sciences Institute, and the Department of Molecular, Cellular and Developmental Biology, University of Michigan, Ann Arbor, MI 48109, United States.
FEBS Lett. 2014 Aug 1;588(15):2457-63. doi: 10.1016/j.febslet.2014.06.015. Epub 2014 Jun 10.
Autophagy as a conserved degradation and recycling process in eukaryotic cells, occurs constitutively, but is induced by stress. A fine regulation of autophagy in space, time, and intensity is critical for maintaining normal energy homeostasis and metabolism, and to allow for its therapeutic modulation in various autophagy-related human diseases. Autophagy activity is regulated in both transcriptional and post-translational manners. In this review, we summarize the cytosolic regulation of autophagy via its molecular machinery, and nuclear regulation by transcription factors. Specifically, we consider Ume6-ATG8 and Pho23-ATG9 transcriptional regulation in detail, as examples of how nuclear transcription factors and cytosolic machinery cooperate to determine autophagosome size and number, which are the two main mechanistic factors through which autophagy activity is regulated.
自噬作为真核细胞中一种保守的降解和回收过程,是持续发生的,但也会被应激诱导。自噬在空间、时间和强度上的精细调节对于维持正常的能量稳态和代谢至关重要,并允许在各种与自噬相关的人类疾病中进行治疗性调节。自噬活性受到转录和翻译后两种方式的调节。在这篇综述中,我们总结了通过其分子机制和转录因子进行的细胞质自噬调节,以及通过核转录因子进行的核自噬调节。具体来说,我们详细考虑了 Ume6-ATG8 和 Pho23-ATG9 的转录调控,以此为例说明核转录因子和细胞质机制如何合作来确定自噬体的大小和数量,这是调节自噬活性的两个主要机制因素。