The P4-type ATPase ATP11C is essential for B lymphopoiesis in adult bone marrow

B lymphopoiesis begins in fetal liver, switching to bone marrow after birth where it persists for life. The unique developmental outcomes of each phase are well documented, yet their molecular requirements are not. Here we describe two allelic X-linked mutations in mice that caused a cell-intrinsic...

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Autores principales: Siggs, Owen M., Arnold, Carrie N., Huber, Christoph, Pirie, Elaine, Xia, Yu, Lin, Pei, Nemazee, David, Beutler, Bruce
Formato: Texto
Lenguaje:English
Publicado: 2011
Materias:
Article
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3079768/
https://www.ncbi.nlm.nih.gov/pubmed/21423172
http://dx.doi.org/10.1038/ni.2012
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author Siggs, Owen M.
Arnold, Carrie N.
Huber, Christoph
Pirie, Elaine
Xia, Yu
Lin, Pei
Nemazee, David
Beutler, Bruce
author_facet Siggs, Owen M.
Arnold, Carrie N.
Huber, Christoph
Pirie, Elaine
Xia, Yu
Lin, Pei
Nemazee, David
Beutler, Bruce
author_sort Siggs, Owen M.
collection PubMed
description B lymphopoiesis begins in fetal liver, switching to bone marrow after birth where it persists for life. The unique developmental outcomes of each phase are well documented, yet their molecular requirements are not. Here we describe two allelic X-linked mutations in mice that caused a cell-intrinsic arrest of adult B lymphopoiesis. Mutant fetal liver progenitors generated B cells in situ, but not in irradiated adult bone marrow, highlighting a necessity for the affected pathway only in the context of adult bone marrow. The causative mutation was ascribed to Atp11c, which encodes a P4-type ATPase with no previously described function. Our data establish an essential, cell-autonomous and context-sensitive function for ATP11C, a putative aminophospholipid flippase, in B cell development.
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spelling pubmed-30797682011-11-01 The P4-type ATPase ATP11C is essential for B lymphopoiesis in adult bone marrow Siggs, Owen M. Arnold, Carrie N. Huber, Christoph Pirie, Elaine Xia, Yu Lin, Pei Nemazee, David Beutler, Bruce Nat Immunol Article B lymphopoiesis begins in fetal liver, switching to bone marrow after birth where it persists for life. The unique developmental outcomes of each phase are well documented, yet their molecular requirements are not. Here we describe two allelic X-linked mutations in mice that caused a cell-intrinsic arrest of adult B lymphopoiesis. Mutant fetal liver progenitors generated B cells in situ, but not in irradiated adult bone marrow, highlighting a necessity for the affected pathway only in the context of adult bone marrow. The causative mutation was ascribed to Atp11c, which encodes a P4-type ATPase with no previously described function. Our data establish an essential, cell-autonomous and context-sensitive function for ATP11C, a putative aminophospholipid flippase, in B cell development. 2011-03-20 2011-05 /pmc/articles/PMC3079768/ /pubmed/21423172 http://dx.doi.org/10.1038/ni.2012 Text en Users may view, print, copy, download and text and data- mine the content in such documents, for the purposes of academic research, subject always to the full Conditions of use: http://www.nature.com/authors/editorial_policies/license.html#terms
spellingShingle Article
Siggs, Owen M.
Arnold, Carrie N.
Huber, Christoph
Pirie, Elaine
Xia, Yu
Lin, Pei
Nemazee, David
Beutler, Bruce
The P4-type ATPase ATP11C is essential for B lymphopoiesis in adult bone marrow
title The P4-type ATPase ATP11C is essential for B lymphopoiesis in adult bone marrow
title_full The P4-type ATPase ATP11C is essential for B lymphopoiesis in adult bone marrow
title_fullStr The P4-type ATPase ATP11C is essential for B lymphopoiesis in adult bone marrow
title_full_unstemmed The P4-type ATPase ATP11C is essential for B lymphopoiesis in adult bone marrow
title_short The P4-type ATPase ATP11C is essential for B lymphopoiesis in adult bone marrow
title_sort p4-type atpase atp11c is essential for b lymphopoiesis in adult bone marrow
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3079768/
https://www.ncbi.nlm.nih.gov/pubmed/21423172
http://dx.doi.org/10.1038/ni.2012
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