Reference: Liu X, et al. (2018) ER-mitochondria contacts are required for pexophagy in Saccharomyces cerevisiae. Contact (Thousand Oaks) 2

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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 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 leads to 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.

Reference Type
Journal Article
Authors
Liu X, Wen X, Klionsky DJ
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