用溶酶体膜(再次)得到PIKy。

Autophagy reports Pub Date : 2024-10-12 eCollection Date: 2024-01-01 DOI:10.1080/27694127.2024.2412916
Alison D Klein, Michael Overholtzer
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引用次数: 0

摘要

关于微自噬及其调控因子,我们仍然知之甚少。在我们最近的论文中,描述了一种微自噬的调节因子,脂质激酶PIKfyve。先前的研究发现,用溶酶性药物或质子离子载体等改变溶酶体渗透电位和pH值的药物治疗细胞,会导致一种选择性降解跨膜蛋白的微自噬。这种微自噬的诱导与溶酶体应激反应有关,溶酶体应激反应涉及巨噬蛋白(如ATG8s)通过一种称为CASM的机制靶向溶酶体膜。我们发现casm诱导的微自噬翻转ATG8和其他溶酶体膜蛋白,并且需要在ATG8脂化下游发挥PIKfyve活性。溶酶体生物发生转录因子TFEB与微自噬平行诱导,以casm依赖性,但不依赖于pik5的方式。这些发现表明,参与CASM的应激源通过微自噬引起选择性翻转,微自噬与溶酶体的生物发生通过一种可通过PIKfyve分离的机制协调。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Getting PIKy with the lysosome membrane (again).

Much is still unknown about microautophagy and its regulators. In our recent paper, one such regulator of microautophagy, the lipid kinase PIKfyve, is described. Previously it was found that treating cells with agents like lysomotropic drugs or proton ionophores, which alter lysosomal osmotic potential and pH, leads to a form of microautophagy that selectively degrades transmembrane proteins. Induction of this type of microautophagy is linked to a lysosomal stress response that involves the targeting of macroautophagy proteins, like ATG8s, to the lysosome membrane, through a mechanism called CASM. We found that CASM-induced microautophagy turns over ATG8s and other lysosomal membrane proteins, and requires PIKfyve activity functioning downstream of ATG8 lipidation. The lysosome biogenesis transcription factor TFEB is induced in parallel to microautophagy, in a CASM-dependent, but PIKfyve-independent manner. These findings demonstrate that stressors that engage CASM cause selective turnover by microautophagy that is coordinated with lysosome biogenesis through a mechanism that is separable through PIKfyve.

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