دورية أكاديمية
أعرض في EDS

Protein import motor complex reacts to mitochondrial misfolding by reducing protein import and activating mitophagy.

التفاصيل البيبلوغرافية
العنوان: Protein import motor complex reacts to mitochondrial misfolding by reducing protein import and activating mitophagy.
المؤلفون: Michaelis JB; Institute of Biochemistry II, Goethe University Frankfurt am Main, Faculty of Medicine, Theodor-Stern-Kai 7, Building 75, 60590, Frankfurt, Germany., Brunstein ME; Institute of Biochemistry II, Goethe University Frankfurt am Main, Faculty of Medicine, Theodor-Stern-Kai 7, Building 75, 60590, Frankfurt, Germany., Bozkurt S; Institute of Biochemistry II, Goethe University Frankfurt am Main, Faculty of Medicine, Theodor-Stern-Kai 7, Building 75, 60590, Frankfurt, Germany., Alves L; Institute of Biochemistry II, Goethe University Frankfurt am Main, Faculty of Medicine, Theodor-Stern-Kai 7, Building 75, 60590, Frankfurt, Germany.; Buchmann Institute for Molecular Life Sciences, Frankfurt am Main, Germany., Wegner M; Institute of Biochemistry II, Goethe University Frankfurt am Main, Faculty of Medicine, Theodor-Stern-Kai 7, Building 75, 60590, Frankfurt, Germany., Kaulich M; Institute of Biochemistry II, Goethe University Frankfurt am Main, Faculty of Medicine, Theodor-Stern-Kai 7, Building 75, 60590, Frankfurt, Germany.; Frankfurt Cancer Institute, Frankfurt am Main, Germany.; Cardio-Pulmonary Institute, Frankfurt am Main, Germany., Pohl C; Institute of Biochemistry II, Goethe University Frankfurt am Main, Faculty of Medicine, Theodor-Stern-Kai 7, Building 75, 60590, Frankfurt, Germany.; Buchmann Institute for Molecular Life Sciences, Frankfurt am Main, Germany.; Discovery Neuroscience, AbbVie Deutschland GmbH & Co KG, Knollstrasse 50, 67061, Ludwigshafen, Germany., Münch C; Institute of Biochemistry II, Goethe University Frankfurt am Main, Faculty of Medicine, Theodor-Stern-Kai 7, Building 75, 60590, Frankfurt, Germany. ch.muench@em.uni-frankfurt.de.; Frankfurt Cancer Institute, Frankfurt am Main, Germany. ch.muench@em.uni-frankfurt.de.; Cardio-Pulmonary Institute, Frankfurt am Main, Germany. ch.muench@em.uni-frankfurt.de.
المصدر: Nature communications [Nat Commun] 2022 Sep 02; Vol. 13 (1), pp. 5164. Date of Electronic Publication: 2022 Sep 02.
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: Nature Pub. Group Country of Publication: England NLM ID: 101528555 Publication Model: Electronic Cited Medium: Internet ISSN: 2041-1723 (Electronic) Linking ISSN: 20411723 NLM ISO Abbreviation: Nat Commun Subsets: MEDLINE
أسماء مطبوعة: Original Publication: [London] : Nature Pub. Group
مواضيع طبية MeSH: Mitophagy* , Protein Kinases*/metabolism, Mitochondria/metabolism ; Mitochondrial Proteins/metabolism ; Ubiquitin-Protein Ligases/metabolism
مستخلص: Mitophagy is essential to maintain mitochondrial function and prevent diseases. It activates upon mitochondria depolarization, which causes PINK1 stabilization on the mitochondrial outer membrane. Strikingly, a number of conditions, including mitochondrial protein misfolding, can induce mitophagy without a loss in membrane potential. The underlying molecular details remain unclear. Here, we report that a loss of mitochondrial protein import, mediated by the pre-sequence translocase-associated motor complex PAM, is sufficient to induce mitophagy in polarized mitochondria. A genome-wide CRISPR/Cas9 screen for mitophagy inducers identifies components of the PAM complex. Protein import defects are able to induce mitophagy without a need for depolarization. Upon mitochondrial protein misfolding, PAM dissociates from the import machinery resulting in decreased protein import and mitophagy induction. Our findings extend the current mitophagy model to explain mitophagy induction upon conditions that do not affect membrane polarization, such as mitochondrial protein misfolding.
(© 2022. The Author(s).)
References: Nat Rev Mol Cell Biol. 2010 Sep;11(9):655-67. (PMID: 20729931)
Mol Cell Biol. 2018 Sep 28;38(20):. (PMID: 30061372)
Biotechniques. 2011 Feb;50(2):98-115. (PMID: 21486251)
iScience. 2020 Dec 31;24(1):102029. (PMID: 33506190)
Biophys J. 2004 Jun;86(6):3993-4003. (PMID: 15189895)
Autophagy. 2020 Mar;16(3):419-434. (PMID: 31177901)
Sci Rep. 2019 Oct 23;9(1):15246. (PMID: 31645584)
Elife. 2017 Apr 25;6:. (PMID: 28440746)
Science. 2015 Sep 25;349(6255):1544-8. (PMID: 26404837)
Genome Res. 2004 Oct;14(10B):2162-8. (PMID: 15489339)
J Microsc. 2006 Dec;224(Pt 3):213-32. (PMID: 17210054)
Nat Commun. 2021 Jan 11;12(1):265. (PMID: 33431889)
Cell Death Dis. 2014 Apr 17;5:e1180. (PMID: 24743735)
Curr Protoc Cell Biol. 2015 Sep 01;68:3.27.1-3.27.33. (PMID: 26331984)
Sci Rep. 2015 Nov 24;5:17154. (PMID: 26598328)
J Biol Chem. 2001 Oct 5;276(40):37327-34. (PMID: 11489896)
Methods. 2003 Aug;30(4):313-21. (PMID: 12828945)
J Cell Biol. 2010 Nov 29;191(5):933-42. (PMID: 21115803)
Nature. 2016 Jun 30;534(7609):710-3. (PMID: 27350246)
Autophagy. 2018;14(10):1693-1709. (PMID: 29938581)
Cell Metab. 2018 Feb 6;27(2):439-449.e5. (PMID: 29337137)
Cell Rep. 2018 Jun 5;23(10):2989-3005. (PMID: 29874585)
Nat Biotechnol. 2016 Feb;34(2):184-191. (PMID: 26780180)
Nat Struct Mol Biol. 2004 Mar;11(3):226-33. (PMID: 14981507)
J Cell Biol. 2003 Jan 20;160(2):189-200. (PMID: 12527753)
Mol Cell. 2022 Jan 20;82(2):435-446.e7. (PMID: 34847359)
Mitochondrion. 2013 Nov;13(6):705-20. (PMID: 23438705)
Am J Hum Genet. 2019 May 2;104(5):784-801. (PMID: 31051112)
Proc Natl Acad Sci U S A. 2006 Apr 18;103(16):6166-71. (PMID: 16606842)
J Am Chem Soc. 2009 Aug 5;131(30):10356-7. (PMID: 19722611)
Front Neurosci. 2018 May 23;12:342. (PMID: 29875626)
PLoS Genet. 2019 May 17;15(5):e1007947. (PMID: 31100073)
Autophagy. 2013 Nov 1;9(11):1750-7. (PMID: 24149988)
Nat Methods. 2014 Mar;11(3):319-24. (PMID: 24487582)
J Cell Biol. 2017 Oct 2;216(10):3231-3247. (PMID: 28893839)
Nat Struct Mol Biol. 2004 Mar;11(3):234-41. (PMID: 14981506)
Mol Cell. 2020 Feb 20;77(4):913-925.e4. (PMID: 31812349)
Clin Cancer Res. 2010 Oct 1;16(19):4779-88. (PMID: 20876793)
Genome Biol. 2014;15(12):554. (PMID: 25476604)
Mol Cell Proteomics. 2018 Dec;17(12):2534-2545. (PMID: 30385480)
Cold Spring Harb Protoc. 2016 Dec 1;2016(12):. (PMID: 27934682)
J Cell Biol. 2008 Dec 1;183(5):795-803. (PMID: 19029340)
Free Radic Biol Med. 2017 Jul;108:236-246. (PMID: 28365360)
Genetics. 1974 May;77(1):71-94. (PMID: 4366476)
Nat Methods. 2012 Mar 04;9(4):357-9. (PMID: 22388286)
Nucleic Acids Res. 2019 Jan 8;47(D1):D442-D450. (PMID: 30395289)
PLoS Biol. 2010 Jan 26;8(1):e1000298. (PMID: 20126261)
PLoS One. 2014 Aug 11;9(8):e104237. (PMID: 25111180)
Mol Biol Cell. 2009 Mar;20(5):1400-7. (PMID: 19144822)
Cell. 2015 Dec 3;163(6):1515-26. (PMID: 26627737)
Blood. 2012 Apr 5;119(14):3321-9. (PMID: 22323447)
Nucleic Acids Res. 2016 Jan 4;44(D1):D1251-7. (PMID: 26450961)
Cells. 2017 Aug 30;6(3):. (PMID: 28867808)
Science. 2022 Jan 14;375(6577):eabi4343. (PMID: 35025629)
Biochim Biophys Acta. 2012 Dec;1823(12):2297-310. (PMID: 22917578)
Science. 2004 May 21;304(5674):1158-60. (PMID: 15087508)
Biochim Biophys Acta. 2012 Sep-Oct;1819(9-10):1098-106. (PMID: 22172993)
Nat Biotechnol. 2018 Oct;36(9):880-887. (PMID: 30125270)
Cell. 2003 Jan 10;112(1):41-50. (PMID: 12526792)
EMBO Rep. 2012 Apr;13(4):378-85. (PMID: 22354088)
Genome Res. 2003 Sep;13(9):2129-41. (PMID: 12952881)
Nature. 2019 Nov;575(7782):375-379. (PMID: 31618756)
EMBO Rep. 2013 Dec;14(12):1127-35. (PMID: 24176932)
Sci Transl Med. 2016 Jun 8;8(342):342ra78. (PMID: 27280685)
J Cell Biol. 2011 Nov 14;195(4):643-56. (PMID: 22065641)
Nat Genet. 2000 Jul;25(3):302-5. (PMID: 10888878)
المشرفين على المادة: 0 (Mitochondrial Proteins)
EC 2.3.2.27 (Ubiquitin-Protein Ligases)
EC 2.7.- (Protein Kinases)
تواريخ الأحداث: Date Created: 20220902 Date Completed: 20220908 Latest Revision: 20220926
رمز التحديث: 20221213
مُعرف محوري في PubMed: PMC9440083
DOI: 10.1038/s41467-022-32564-x
PMID: 36056001
قاعدة البيانات: MEDLINE
الوصف
تدمد:2041-1723
DOI:10.1038/s41467-022-32564-x