Abstract
The molecular determinants of spleen organogenesis and the etiology of isolated congenital asplenia (ICA), a life-threatening human condition, are unknown. We previously reported that Pbx1 deficiency causes organ growth defects including asplenia. Here, we show that mice with splenic mesenchyme-specific Pbx1 inactivation exhibit hyposplenia. Moreover, the loss of Pbx causes downregulation of Nkx2-5 and derepression of p15Ink4b in spleen mesenchymal progenitors, perturbing the cell cycle. Removal of p15Ink4b in Pbx1 spleen-specific mutants partially rescues spleen growth. By whole-exome sequencing of a multiplex kindred with ICA, we identify a heterozygous missense mutation (P236H) in NKX2-5 showing reduced transactivation in vitro. This study establishes that a Pbx/Nkx2-5/p15 regulatory module is essential for spleen development.
Copyright © 2012 Elsevier Inc. All rights reserved.
Publication types
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Case Reports
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Adolescent
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Amino Acid Sequence
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Animals
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Cells, Cultured
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Cyclin-Dependent Kinase Inhibitor p15 / metabolism
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DNA-Binding Proteins / deficiency
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Exome
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Female
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Gene Expression Profiling
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Gene Expression Regulation, Developmental
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Homeobox Protein Nkx-2.5
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Homeodomain Proteins / genetics*
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Homeodomain Proteins / metabolism
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Humans
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Infant
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Male
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Mice
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Mice, Transgenic
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Molecular Sequence Data
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Mutation, Missense
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Pedigree
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Pre-B-Cell Leukemia Transcription Factor 1
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Proto-Oncogene Proteins / deficiency
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Spleen / abnormalities*
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Splenic Diseases / genetics*
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Transcription Factors / deficiency
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Transcription Factors / genetics*
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Transcription Factors / metabolism
Substances
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CDKN2B protein, human
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Cdkn2b protein, mouse
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Cyclin-Dependent Kinase Inhibitor p15
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DNA-Binding Proteins
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Homeobox Protein Nkx-2.5
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Homeodomain Proteins
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NKX2-5 protein, human
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Nkx2-5 protein, mouse
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Pbx1 protein, mouse
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Pre-B-Cell Leukemia Transcription Factor 1
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Proto-Oncogene Proteins
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Transcription Factors
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PBX1 protein, human