Journal
NATURE IMMUNOLOGY
Volume 12, Issue 5, Pages 434-U89Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ni.2012
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Funding
- Bill & Melinda Gates Foundation
- National Institute of Allergy and Infectious Diseases of the National Institutes of Health [HHSN272200700038C]
- General Sir John Monash Foundation
- Cancer Research Institute
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B lymphopoiesis begins in the fetal liver, switching after birth to the bone marrow, 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 cell-intrinsic arrest of adult B lymphopoiesis. Mutant fetal liver progenitors generated B cells in situ but not in irradiated adult bone marrow, which emphasizes a necessity for the affected pathway only in the context of adult bone marrow. The causative mutations were 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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