دورية أكاديمية
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Orthogonal Targeting of SAC1 to Mitochondria Implicates ORP2 as a Major Player in PM PI4P Turnover.

التفاصيل البيبلوغرافية
العنوان: Orthogonal Targeting of SAC1 to Mitochondria Implicates ORP2 as a Major Player in PM PI4P Turnover.
المؤلفون: Doyle CP; Department of Cell Biology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261, USA., Rectenwald A; Department of Cell Biology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261, USA., Timple L; Department of Cell Biology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261, USA., Hammond GRV; Department of Cell Biology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261, USA.
المصدر: Contact (Thousand Oaks (Ventura County, Calif.)) [Contact (Thousand Oaks)] 2024 Feb 07; Vol. 7, pp. 25152564241229272. Date of Electronic Publication: 2024 Feb 07 (Print Publication: 2024).
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Sage Publications Country of Publication: United States NLM ID: 101729710 Publication Model: eCollection Cited Medium: Internet ISSN: 2515-2564 (Electronic) Linking ISSN: 25152564 NLM ISO Abbreviation: Contact (Thousand Oaks) Subsets: PubMed not MEDLINE
أسماء مطبوعة: Original Publication: [Thousand Oaks, California] : Sage Publications, [2018]-
مستخلص: Oxysterol-binding protein (OSBP)-related proteins (ORPs) 5 and 8 have been shown to deplete the lipid phosphatidylinositol 4-phosphate (PI4P) at sites of membrane contact between the endoplasmic reticulum (ER) and plasma membrane (PM). This is believed to be caused by transport of PI4P from the PM to the ER, where PI4P is degraded by an ER-localized SAC1 phosphatase. This is proposed to power the anti-port of phosphatidylserine (PS) lipids from ER to PM, up their concentration gradient. Alternatively, ORPs have been proposed to sequester PI4P, dependent on the concentration of their alternative lipid ligand. Here, we aimed to distinguish these possibilities in living cells by orthogonal targeting of PI4P transfer and degradation to PM-mitochondria contact sites. Surprisingly, we found that orthogonal targeting of SAC1 to mitochondria enhanced PM PI4P turnover independent of targeting to contact sites with the PM. This turnover could be slowed by knock-down of soluble ORP2, which also has a major impact on PM PI4P levels even without SAC1 over-expression. The data reveal a role for contact site-independent modulation of PM PI4P levels and lipid antiport.
Competing Interests: The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
(© The Author(s) 2024.)
التعليقات: Update of: bioRxiv. 2024 Jan 11;:. (PMID: 37693626)
References: J Cell Sci. 2004 Mar 1;117(Pt 7):1201-10. (PMID: 14996942)
Exp Cell Res. 2018 Sep 15;370(2):601-612. (PMID: 30028970)
Methods Mol Biol. 2021;2251:55-72. (PMID: 33481231)
BMC Biol. 2021 Nov 20;19(1):248. (PMID: 34801011)
Biochem J. 2022 Nov 11;479(21):2311-2325. (PMID: 36367756)
PLoS Pathog. 2015 Jun 12;11(6):e1004965. (PMID: 26067986)
J Cell Biol. 2011 Dec 12;195(6):965-78. (PMID: 22162133)
Traffic. 2010 Sep;11(9):1180-90. (PMID: 20573065)
EMBO J. 2017 Nov 2;36(21):3156-3174. (PMID: 28978670)
Nat Commun. 2019 Sep 2;10(1):3926. (PMID: 31477717)
J Cell Biol. 2014 Apr 14;205(1):113-26. (PMID: 24711504)
Biochem J. 2009 Jul 29;422(1):23-35. (PMID: 19508231)
Cell. 2013 Nov 7;155(4):830-43. (PMID: 24209621)
Science. 2015 Jul 24;349(6246):432-6. (PMID: 26206936)
Biochimie. 2019 Mar;158:90-101. (PMID: 30590084)
Prog Lipid Res. 2022 Apr;86:101146. (PMID: 34999137)
J Cell Biol. 2018 May 7;217(5):1797-1813. (PMID: 29472386)
Science. 2012 Aug 10;337(6095):727-30. (PMID: 22722250)
Cell Rep. 2013 Nov 14;5(3):813-25. (PMID: 24183667)
Nat Commun. 2017 Oct 2;8(1):757. (PMID: 28970484)
Science. 2015 Jul 24;349(6246):428-32. (PMID: 26206935)
Curr Opin Cell Biol. 2019 Aug;59:58-72. (PMID: 31039522)
EMBO J. 2003 May 1;22(9):2025-35. (PMID: 12727870)
Front Mol Biosci. 2021 Oct 12;8:747601. (PMID: 34712698)
Cell Tissue Res. 2004 Jan;315(1):39-57. (PMID: 14593528)
Proc Natl Acad Sci U S A. 2016 Apr 19;113(16):4314-9. (PMID: 27044099)
Elife. 2018 Feb 20;7:. (PMID: 29461204)
J Biol Chem. 2014 Feb 28;289(9):6120-32. (PMID: 24415756)
EMBO J. 2021 Jul 15;40(14):e106871. (PMID: 34124795)
Cell Calcium. 2005 Feb;37(2):129-36. (PMID: 15589993)
Proc Natl Acad Sci U S A. 2012 Aug 28;109(35):E2316-23. (PMID: 22847441)
mBio. 2014 Jan 28;5(1):e00839-13. (PMID: 24473127)
Science. 2022 Mar 11;375(6585):eabi6983. (PMID: 35271311)
Nat Rev Mol Cell Biol. 2020 Jan;21(1):7-24. (PMID: 31732717)
J Cell Biol. 2020 Mar 2;219(3):. (PMID: 32211893)
Mol Cell. 2019 Feb 7;73(3):458-473.e7. (PMID: 30581148)
J Biol Chem. 2000 Nov 3;275(44):34293-305. (PMID: 10887188)
J Cell Sci. 2023 Aug 15;136(16):. (PMID: 37534432)
Traffic. 2011 Feb;12(2):218-31. (PMID: 21062391)
Nat Rev Mol Cell Biol. 2019 Feb;20(2):85-101. (PMID: 30337668)
معلومات مُعتمدة: R35 GM119412 United States GM NIGMS NIH HHS
فهرسة مساهمة: Keywords: PtdIns4P; lipid transfer proteins; membrane contact sites; phosphoinositides
تواريخ الأحداث: Date Created: 20240208 Latest Revision: 20240219
رمز التحديث: 20240219
مُعرف محوري في PubMed: PMC10848804
DOI: 10.1177/25152564241229272
PMID: 38327560
قاعدة البيانات: MEDLINE
الوصف
تدمد:2515-2564
DOI:10.1177/25152564241229272