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ROS transfer at peroxisome-mitochondria contact sites maintains mitochondrial redox homeostasis

ABSTRACT: Data deposited contain results from proximity-dependent biotinylation LC-MS (BioID) experiments in which T-REx Flp-In HEK293 cells express ACBD5 or PTPIP51 proteins fused to biotin carboxylase BirA.

INSTRUMENT(S): Q Exactive HF

ORGANISM(S): Homo Sapiens (ncbitaxon:9606)

SUBMITTER: Brian Raught

PROVIDER: MSV000093219 | MassIVE | Wed Nov 01 06:49:00 GMT 2023

SECONDARY ACCESSION(S): PXD046577

REPOSITORIES: MassIVE

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ROS transfer at peroxisome-mitochondria contact regulates mitochondrial redox.

DiGiovanni Laura F LF Khroud Prabhsimran K PK Carmichael Ruth E RE Schrader Tina A TA Gill Shivneet K SK Germain Kyla K Jomphe Robert Y RY Wiesinger Christoph C Boutry Maxime M Kamoshita Maki M Snider Daniel D Stubbings Garret G Hua Rong R Garber Noel N Hacker Christian C Rutenberg Andrew D AD Melnyk Roman A RA Berger Johannes J Schrader Michael M Raught Brian B Kim Peter K PK

Science (New York, N.Y.) 20250710 6756

Maintenance of mitochondrial redox homeostasis is of fundamental importance to cellular health. Mitochondria harbor a host of intrinsic antioxidant defenses, but the contribution of extrinsic, nonmitochondrial antioxidant mechanisms is less well understood. We found a direct role for peroxisomes in maintaining mitochondrial redox homeostasis through contact-mediated reactive oxygen species (ROS) transfer. We found that ACBD5 and PTPIP51 form a contact between peroxisomes and mitochondria. The pe ...[more]

PMID: 40638754

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