醉酒进食：毒素 MakA 调控自噬的分子机制特征。

Eating while intoxicated: characterizing the molecular mechanism behind toxin MakA-regulated autophagy.

机构信息

Department of Chemistry, Umeå University, Umeå, Sweden.

Umeå Centre for Microbial Research, Umeå University, Umeå, Sweden.

出版信息

Autophagy. 2023 Jun;19(6):1885-1886. doi: 10.1080/15548627.2022.2146893. Epub 2022 Nov 21.

DOI:10.1080/15548627.2022.2146893

PMID:36409136

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10262753/

Abstract

Extracellular pathogens utilize secreted virulence factors to regulate host cell function. Recently we characterized the molecular mechanism behind host macroautophagy/autophagy regulation by the toxin MakA. Cholesterol binding at the plasma membrane induces MakA endocytosis and pH-dependent pore assembly. Membrane perforation of late endosomal membranes induces cellular membrane repair pathways and V-ATPase-dependent unconventional LC3 lipidation on damaged membranes.

摘要

细胞外病原体利用分泌的毒力因子来调节宿主细胞功能。最近，我们描述了 MakA 毒素调控宿主巨自噬/自噬的分子机制。细胞膜上胆固醇的结合诱导 MakA 的内吞作用和 pH 依赖性孔组装。晚期内体膜的膜穿孔诱导细胞的膜修复途径和 V-ATPase 依赖性受损膜上的非典型 LC3 脂质化。