Critical Role of Lipid Scramblase TMEM16F in Phosphatidylserine Exposure and Repair of Plasma Membrane after Pore Formation.
Animals
Anoctamins
/ genetics
Bacterial Toxins
/ toxicity
Calcium
/ metabolism
Cell Death
/ drug effects
Cell Membrane
/ drug effects
Extracellular Vesicles
/ drug effects
Heat-Shock Proteins
/ toxicity
Hemolysin Proteins
/ toxicity
Listeria monocytogenes
/ metabolism
Liver
/ cytology
Membrane Lipids
/ metabolism
Mice
Mice, Inbred C57BL
Mice, Knockout
Microscopy, Electron, Scanning
Neutrophils
/ cytology
Phosphatidylserines
/ metabolism
Phospholipid Transfer Proteins
/ genetics
Spleen
/ cytology
Thymocytes
/ drug effects
ANO6
Listeria
TMEM16F
calcium
extracellular vesicles
lipid scrambling
listeriolysin O
phosphatidylserine exposure
plasma membrane repair
pore forming
scramblase
Journal
Cell reports
ISSN: 2211-1247
Titre abrégé: Cell Rep
Pays: United States
ID NLM: 101573691
Informations de publication
Date de publication:
28 01 2020
28 01 2020
Historique:
received:
22
07
2019
revised:
25
10
2019
accepted:
17
12
2019
entrez:
30
1
2020
pubmed:
30
1
2020
medline:
21
10
2020
Statut:
ppublish
Résumé
Plasma membrane damage and cell death during processes such as necroptosis and apoptosis result from cues originating intracellularly. However, death caused by pore-forming agents, like bacterial toxins or complement, is due to direct external injury to the plasma membrane. To prevent death, the plasma membrane has an intrinsic repair ability. Here, we found that repair triggered by pore-forming agents involved TMEM16F, a calcium-activated lipid scramblase also mutated in Scott's syndrome. Upon pore formation and the subsequent influx of intracellular calcium, TMEM16F induced rapid "lipid scrambling" in the plasma membrane. This response was accompanied by membrane blebbing, extracellular vesicle release, preserved membrane integrity, and increased cell viability. TMEM16F-deficient mice exhibited compromised control of infection by Listeria monocytogenes associated with a greater sensitivity of neutrophils to the pore-forming Listeria toxin listeriolysin O (LLO). Thus, the lipid scramblase TMEM16F is critical for plasma membrane repair after injury by pore-forming agents.
Identifiants
pubmed: 31995754
pii: S2211-1247(19)31723-1
doi: 10.1016/j.celrep.2019.12.066
pmc: PMC7104872
mid: NIHMS1553319
pii:
doi:
Substances chimiques
ANO6 protein, human
0
Anoctamins
0
Bacterial Toxins
0
Heat-Shock Proteins
0
Hemolysin Proteins
0
Membrane Lipids
0
Phosphatidylserines
0
Phospholipid Transfer Proteins
0
hlyA protein, Listeria monocytogenes
R06ZRQ1YX9
Calcium
SY7Q814VUP
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
1129-1140.e5Subventions
Organisme : NIDA NIH HHS
ID : DP1 DA038017
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI148080
Pays : United States
Organisme : NCATS NIH HHS
ID : UL1 TR001425
Pays : United States
Organisme : CIHR
ID : MT-14429
Pays : Canada
Organisme : CIHR
ID : MOP-82906
Pays : Canada
Organisme : CIHR
ID : FDN-143338
Pays : Canada
Organisme : CIHR
ID : MOP-142333
Pays : Canada
Organisme : CIHR
ID : PJT-152988
Pays : Canada
Informations de copyright
Copyright © 2019 The Author(s). Published by Elsevier Inc. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of Interests A.V. received a contract from Bristol Myers-Squibb to study the mechanism of action of the anti-SLAMF7 monoclonal antibody elotuzumab in multiple myeloma.
Références
Cell Physiol Biochem. 2007;20(6):1051-60
pubmed: 17975307
Immunity. 2002 Mar;16(3):417-28
pubmed: 11911826
Trends Cell Biol. 2008 Nov;18(11):552-9
pubmed: 18848451
Cell. 2017 Apr 6;169(2):286-300.e16
pubmed: 28388412
Biochem Pharmacol. 2011 Mar 15;81(6):703-12
pubmed: 21219882
Am J Physiol Cell Physiol. 2013 Apr 15;304(8):C748-59
pubmed: 23426967
Cell Mol Life Sci. 2019 Apr;76(7):1319-1339
pubmed: 30591958
J Bone Miner Res. 2013 Feb;28(2):246-59
pubmed: 22936354
Immunity. 2012 Jun 29;36(6):974-85
pubmed: 22683124
Proc Natl Acad Sci U S A. 2019 Jan 22;116(4):1309-1318
pubmed: 30622179
J Biol Chem. 2015 Mar 6;290(10):6270-80
pubmed: 25589784
Science. 2018 Nov 23;362(6417):956-960
pubmed: 30467171
Trends Microbiol. 2012 Aug;20(8):360-8
pubmed: 22652164
Blood. 2010 Feb 25;115(8):1582-93
pubmed: 20038786
Nature. 2014 May 8;509(7499):230-4
pubmed: 24739967
J Cell Sci. 2011 Jul 15;124(Pt 14):2414-23
pubmed: 21693578
Immunity. 2005 Sep;23(3):249-62
pubmed: 16169498
Subcell Biochem. 2014;80:161-95
pubmed: 24798012
Sci Rep. 2019 Jan 24;9(1):619
pubmed: 30679690
Methods Enzymol. 2014;544:381-93
pubmed: 24974298
J Immunol. 2016 Sep 1;197(5):1557-65
pubmed: 27543669
Nature. 2010 Dec 9;468(7325):834-8
pubmed: 21107324
Science. 2014 Feb 28;343(6174):1247136
pubmed: 24482116
Science. 2013 Jul 26;341(6144):403-6
pubmed: 23845944
Cytometry. 1996 Jun 1;24(2):131-9
pubmed: 8725662
Proc Natl Acad Sci U S A. 2015 Oct 13;112(41):12800-5
pubmed: 26417084
Curr Biol. 2018 Apr 23;28(8):R392-R397
pubmed: 29689221
J Immunol. 2008 Jul 15;181(2):1365-74
pubmed: 18606691
Elife. 2019 Jul 18;8:
pubmed: 31318330
J Biol Chem. 2018 Apr 27;293(17):6230-6240
pubmed: 29588369
Nat Immunol. 2015 Sep;16(9):907-17
pubmed: 26287597
Curr Protoc Pharmacol. 2004 Sep 1;Chapter 12:Unit 12.8
pubmed: 22294120
Nature. 2017 Apr 27;544(7651):493-497
pubmed: 28424516
Hum Mol Genet. 2016 May 15;25(10):1900-1911
pubmed: 26911675
Toxins (Basel). 2018 Sep 25;10(10):
pubmed: 30257425
Sci Transl Med. 2015 Nov 25;7(315):315ra190
pubmed: 26606969
Cell. 2012 Sep 28;151(1):111-22
pubmed: 23021219
J Exp Med. 2016 Nov 14;213(12):2759-2772
pubmed: 27810927
Cell Rep. 2016 Jun 21;15(12):2608-15
pubmed: 27332874
Am J Hum Genet. 2010 Feb 12;86(2):213-21
pubmed: 20096397
Annu Rev Physiol. 2017 Feb 10;79:119-143
pubmed: 27860832
Nat Immunol. 2009 Sep;10(9):973-80
pubmed: 19648922
Nat Rev Microbiol. 2018 Jan;16(1):32-46
pubmed: 29176582
Nat Immunol. 2016 Apr;17(4):387-96
pubmed: 26878112
Biophys Rev. 2018 Oct;10(5):1337-1348
pubmed: 30117093
Vox Sang. 2011 Feb;100(2):187-95
pubmed: 20738837