ROS transfer at peroxisome-mitochondria contact regulates mitochondrial redox

IF 45.8 1区综合性期刊 Q1 MULTIDISCIPLINARY SCIENCES

Science Pub Date : 2025-07-10 DOI:10.1126/science.adn2804

Laura F. DiGiovanni, Prabhsimran K. Khroud, Ruth E. Carmichael, Tina A. Schrader, Shivneet K. Gill, Kyla Germain, Robert Y. Jomphe, Christoph Wiesinger, Maxime Boutry, Maki Kamoshita, Daniel Snider, Garret Stubbings, Rong Hua, Noel Garber, Christian Hacker, Andrew D. Rutenberg, Roman A. Melnyk, Johannes Berger, Michael Schrader, Brian Raught, Peter K. Kim

{"title":"ROS transfer at peroxisome-mitochondria contact regulates mitochondrial redox","authors":"Laura F. DiGiovanni, Prabhsimran K. Khroud, Ruth E. Carmichael, Tina A. Schrader, Shivneet K. Gill, Kyla Germain, Robert Y. Jomphe, Christoph Wiesinger, Maxime Boutry, Maki Kamoshita, Daniel Snider, Garret Stubbings, Rong Hua, Noel Garber, Christian Hacker, Andrew D. Rutenberg, Roman A. Melnyk, Johannes Berger, Michael Schrader, Brian Raught, Peter K. Kim","doi":"10.1126/science.adn2804","DOIUrl":null,"url":null,"abstract":"<div >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 percentage of these contacts increased during mitochondrial oxidative stress and helped to maintain mitochondrial health through the transfer of mitochondrial ROS to the peroxisome lumen. Our findings reveal a multiorganelle layer of mitochondrial antioxidant defense—suggesting a direct mechanism by which peroxisomes contribute to mitochondrial health—and broaden the scope of known membrane contact site functions.</div>","PeriodicalId":21678,"journal":{"name":"Science","volume":"389 6756","pages":""},"PeriodicalIF":45.8000,"publicationDate":"2025-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Science","FirstCategoryId":"103","ListUrlMain":"https://www.science.org/doi/10.1126/science.adn2804","RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"MULTIDISCIPLINARY SCIENCES","Score":null,"Total":0}

引用次数: 0

Abstract

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 percentage of these contacts increased during mitochondrial oxidative stress and helped to maintain mitochondrial health through the transfer of mitochondrial ROS to the peroxisome lumen. Our findings reveal a multiorganelle layer of mitochondrial antioxidant defense—suggesting a direct mechanism by which peroxisomes contribute to mitochondrial health—and broaden the scope of known membrane contact site functions.

查看原文本刊更多论文

过氧化物酶体与线粒体接触时ROS的转移调节线粒体氧化还原

线粒体氧化还原稳态的维持对细胞健康至关重要。线粒体拥有许多内在的抗氧化防御，但外在的非线粒体抗氧化机制的作用尚不清楚。我们发现过氧化物酶体通过接触介导的活性氧（ROS）转移在维持线粒体氧化还原稳态中起直接作用。我们发现ACBD5和PTPIP51在过氧化物酶体和线粒体之间形成一种接触。这些接触的百分比在线粒体氧化应激期间增加，并通过将线粒体活性氧转移到过氧化物酶体管腔来帮助维持线粒体健康。我们的研究结果揭示了线粒体抗氧化防御的多细胞器层，这表明过氧化物酶体促进线粒体健康的直接机制，并扩大了已知膜接触部位功能的范围。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文求助全文

来源期刊

Science 综合性期刊-综合性期刊

CiteScore

61.10

自引率

0.90%

发文量

审稿时长

2.1 months

期刊介绍： Science is a leading outlet for scientific news, commentary, and cutting-edge research. Through its print and online incarnations, Science reaches an estimated worldwide readership of more than one million. Science’s authorship is global too, and its articles consistently rank among the world's most cited research. Science serves as a forum for discussion of important issues related to the advancement of science by publishing material on which a consensus has been reached as well as including the presentation of minority or conflicting points of view. Accordingly, all articles published in Science—including editorials, news and comment, and book reviews—are signed and reflect the individual views of the authors and not official points of view adopted by AAAS or the institutions with which the authors are affiliated. Science seeks to publish those papers that are most influential in their fields or across fields and that will significantly advance scientific understanding. Selected papers should present novel and broadly important data, syntheses, or concepts. They should merit recognition by the wider scientific community and general public provided by publication in Science, beyond that provided by specialty journals. Science welcomes submissions from all fields of science and from any source. The editors are committed to the prompt evaluation and publication of submitted papers while upholding high standards that support reproducibility of published research. Science is published weekly; selected papers are published online ahead of print.