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• W2910551587 abstract "Peroxisomes play important roles in lipid metabolism. Surplus or damaged peroxisomes can be selectively targeted for autophagic degradation, a process termed pexophagy. Maintaining a proper level of pexophagy is critical for cellular homeostasis. Here, we found that endoplasmic reticulum (ER)–mitochondria contact sites are necessary for efficient pexophagy. During pexophagy, the peroxisomes destined for degradation are adjacent to the ER–mitochondria encounter structure (ERMES) that mediates the formation of ER–mitochondria contacts; disruption of the ERMES results in a severe defect in pexophagy. We show that a mutant form of Mdm34, a component of the ERMES, which impairs ERMES formation and diminishes its association with the peroxisomal membrane protein Pex11, also causes defects in pexophagy. The dynamin-related GTPase Vps1, which is specific for peroxisomal fission, is recruited to the peroxisomes at ER–mitochondria contacts by the selective autophagy scaffold Atg11 and the pexophagy receptor Atg36, facilitating peroxisome degradation." @default.
• W2910551587 created "2019-01-25" @default.
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• W2910551587 date "2019-01-01" @default.
• W2910551587 modified "2023-10-18" @default.
• W2910551587 title "Endoplasmic Reticulum–Mitochondria Contacts Are Required for Pexophagy in <i>Saccharomyces cerevisiae</i>" @default.
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• W2910551587 doi "https://doi.org/10.1177/2515256418821584" @default.
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