PERK Signaling Promotes Mitochondrial Elongation By Remodeling Membrane Phosphatidic Acid

ABSTRACT: Endoplasmic reticulum (ER) stress and mitochondrial dysfunction are linked in the onset and pathogenesis of numerous diseases. This has led to considerable interest in defining the mechanisms responsible for regulating mitochondria during ER stress. The PERK signaling arm of the unfolded protein response (UPR) has emerged as a prominent ER stress-responsive signaling pathway that regulates diverse aspects of mitochondrial biology. Here, we show that PERK activity promotes adaptive remodeling of mitochondrial membrane phosphatidic acid (PA) to induce protective mitochondrial elongation during acute ER stress. We find that PERK activity is required for ER stress-dependent increases in both cellular PA and YME1L-dependent degradation of the intramitochondrial PA transporter PRELID1. These two

SUBMITTER: Ms. Valerie Perea 

PROVIDER: S-SCDT-10_15252-EMBJ_2023113908 | biostudies-other |

REPOSITORIES: biostudies-other