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Mice deficient in the putative phospholipid flippase ATP11C exhibit altered erythrocyte shape, anemia, and reduced erythrocyte life span

Yabas, Mehmet; Coupland, Lucy A; Cromer, Deborah; Winterberg, Markus; Teoh, Narci C; D'Rozario, James; Kirk, Kiaran; Bröer, Stefan; Parish, Christopher; Enders, Anselm

Description

Transmembrane lipid transporters are believed to establish and maintain phospholipid asymmetry in biological membranes; however, little is known about the in vivo function of the specific transporters involved. Here, we report that developing erythrocytes from mice lacking the putative phosphatidylserine flippase ATP11Cshowed a lower rate ofPStranslocation in vitro compared with erythrocytes from wild-type littermates. Furthermore, the mutant mice had an elevated percentage of...[Show more]

dc.contributor.authorYabas, Mehmet
dc.contributor.authorCoupland, Lucy A
dc.contributor.authorCromer, Deborah
dc.contributor.authorWinterberg, Markus
dc.contributor.authorTeoh, Narci C
dc.contributor.authorD'Rozario, James
dc.contributor.authorKirk, Kiaran
dc.contributor.authorBröer, Stefan
dc.contributor.authorParish, Christopher
dc.contributor.authorEnders, Anselm
dc.date.accessioned2015-01-16T01:26:55Z
dc.date.available2015-01-16T01:26:55Z
dc.identifier.issn0021-9258
dc.identifier.urihttp://hdl.handle.net/1885/12545
dc.description.abstractTransmembrane lipid transporters are believed to establish and maintain phospholipid asymmetry in biological membranes; however, little is known about the in vivo function of the specific transporters involved. Here, we report that developing erythrocytes from mice lacking the putative phosphatidylserine flippase ATP11Cshowed a lower rate ofPStranslocation in vitro compared with erythrocytes from wild-type littermates. Furthermore, the mutant mice had an elevated percentage of phosphatidylserineexposing mature erythrocytes in the periphery. Although erythrocyte development in ATP11C-deficient mice was normal, the mature erythrocytes had an abnormal shape (stomatocytosis), and the life span of mature erythrocytes was shortened relative to that in control littermates, resulting in anemia in the mutant mice. Thus, our findings uncover an essential role for ATP11C in erythrocyte morphology and survival and provide a new candidate for the rare inherited blood disorder stomatocytosis with uncompensated anemia.
dc.description.sponsorshipThis work was supported in part by National Health and Medical Research Council Grant GNT1061288. Supported by National Health and Medical Research Council Career Development Fellowship GNT1035858 and by the Ramaciotti Foundation.
dc.format8 pages
dc.publisherAmerican Society for Biochemistry and Molecular Biology
dc.rights© 2014 by The American Society for Biochemistry and Molecular Biology, Inc. Subject to 12 month restriction, author may post accepted version to institutional repository http://www.sherpa.ac.uk/romeo/issn/0021-9258/ Sherpa/Romeo as at 3 June 2015
dc.sourceJournal of Biological Chemistry 289.28 (2014): 19531-19537
dc.subjectmice
dc.subjectphospholipid
dc.subjectflippase
dc.subjectATP11C
dc.subjectlife span
dc.titleMice deficient in the putative phospholipid flippase ATP11C exhibit altered erythrocyte shape, anemia, and reduced erythrocyte life span
dc.typeJournal article
local.identifier.citationvolume289
dc.date.issued2014-06-04
local.identifier.absfor060199 - Biochemistry and Cell Biology not elsewhere classified
local.identifier.ariespublicationu6800332xPUB230
local.publisher.urlhttp://www.asbmb.org/
local.type.statusAccepted version
local.contributor.affiliationYabas, Mehmet, Ramaciotti Immunization Genomics Laboratory, The John Curtin School of Medical Research, The Australian National University
local.contributor.affiliationCoupland, Lucy A, Cancer and Vascular Biology Group, Department of Immunology, The John Curtin School of Medical Research, The Australian National University and Clinical Haematology Unit, The Canberra Hospital
local.contributor.affiliationCromer, Deborah, Complex Systems in Biology Group, Centre for Vascular Research, University of New South Wales
local.contributor.affiliationWinterberg, Markus, Division of Biomedical Science and Biochemistry, Research School of Biology, The Australian National University
local.contributor.affiliationTeoh, Narci C., Liver Research Group, The Australian National University Medical School at the Canberra Hospital
local.contributor.affiliationD’Rozario, James, Clinical Haematology Unit, The Canberra Hospital
local.contributor.affiliationKirk, Kiaran, Division of Biomedical Science and Biochemistry, Research School of Biology, The Australian National University
local.contributor.affiliationBröer, Stefan, Division of Biomedical Science and Biochemistry, Research School of Biology, The Australian National University
local.contributor.affiliationParish, Christopher R., Cancer and Vascular Biology Group, Department of Immunology, The John Curtin School of Medical Research, The Australian National University
local.contributor.affiliationEnders, Anlsem, Ramaciotti Immunization Genomics Laboratory, The John Curtin School of Medical Research, The Australian National University
dc.relationhttp://purl.org/au-research/grants/nhmrc/1061288
dc.relationhttp://purl.org/au-research/grants/nhmrc/1035858
local.identifier.essn1083-351X
local.bibliographicCitation.issue28
local.bibliographicCitation.startpage19531
local.bibliographicCitation.lastpage19537
local.identifier.doi10.1074/jbc.C114.570267
dc.date.updated2015-12-09T08:41:15Z
local.identifier.scopusID2-s2.0-84904171129
local.identifier.thomsonID000339326800028
CollectionsANU Research Publications

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