该留还是该走:间隙连接蛋白 GJA1/Cx43 将受损的溶酶体输送到细胞外围,以增强外吞作用。

Autophagy Pub Date : 2024-12-01 Epub Date: 2024-10-21 DOI:10.1080/15548627.2024.2408711
Neuza Domingues, Teresa Ribeiro-Rodrigues, Henrique Girão
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引用次数: 0

摘要

长期以来,GJA1/Cx43(间隙连接蛋白α1)一直与间隙连接介导的相邻细胞间的通讯有关。然而,最近的数据打破了这一概念,研究表明 GJA1 与其他生物过程有关,如大自噬/自噬调节、线粒体活性和细胞外囊泡生物学。在我们最近的研究中,我们揭示了 GJA1 在溶酶体转运中扮演的另一个角色。我们证明,GJA1 通过依赖 ACTR2/ARP2-ACTR3/ARP3 的肌动蛋白重塑机制,促进受损溶酶体的外排。我们的研究结果表明,GJA1 在病原体感染和溶酶体贮存紊乱过程中发挥着重要作用,有利于功能障碍溶酶体的释放。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Should it stay or should it go: gap junction protein GJA1/Cx43 conveys damaged lysosomes to the cell periphery to potentiate exocytosis.

GJA1/Cx43 (gap junction protein alpha 1) has long been associated with gap junctions-mediated communication between adjacent cells. However, recent data have defied this concept, with studies implicating GJA1 in other biological processes, such as macroautophagy/autophagy regulation, mitochondrial activity and extracellular vesicles biology. In our recent study we unveiled an additional role played by GJA1 in lysosomal trafficking. We demonstrate that GJA1 promotes the exocytosis of damaged lysosomes, through a mechanism that relies on ACTR2/ARP2-ACTR3/ARP3-dependent actin remodeling. Our findings ascribe to GJA1 an important role during pathogen infection and lysosomal storage disorders, favoring the release of dysfunctional lysosomes.

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