Deficient Alk3-mediated BMP signaling causes prenatal omphalocele-like defect

Jianping Sun; Yi-Hsin Liu; Hui Chen; Manuel P Nguyen; Yuji Mishina; Jeffrey S Upperman; Henri R Ford; Wei Shi

doi:10.1016/j.bbrc.2007.06.049

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Deficient Alk3-mediated BMP signaling causes prenatal omphalocele-like defect

Journal article

Open access

Peer reviewed

Deficient Alk3-mediated BMP signaling causes prenatal omphalocele-like defect

Jianping Sun, Yi-Hsin Liu, Hui Chen, Manuel P Nguyen, Yuji Mishina, Jeffrey S Upperman, Henri R Ford and Wei Shi

Biochemical and biophysical research communications, Vol.360(1), pp.238-243

2007

DOI: https://doi.org/10.1016/j.bbrc.2007.06.049

PMCID: PMC1987715

PMID: 17588538

Abstract

Alk3

BMP

Omphalocele

Ventral body wall

BMP signaling plays important roles in many embryonic developmental processes. Alk3 is one of two BMP type I receptors that transduces BMP signal from the cell surface into cell. Conventional knockout of Alk3 resulted in early embryonic lethality around E7.5–E9.5. In this study, we have generated embryonic mesoderm-specific Alk3 conditional knockout by crossing Dermo1-Cre and floxed Alk3 mice. Abrogation of Alk3-mediated BMP signaling in this mouse resulted in severe defect of secondary ventral body wall formation, replicating the omphalocele phenotype in human. Our finding suggests that Alk3 plays an essential role in the formation of embryonic ventral abdominal wall, and abrogation of BMP signaling activity due to gene mutations in its signaling components could be one of the underlying causes of omphalocele at birth.

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Collaboration types: Domestic collaboration
Citation topics: 1 Clinical & Life Sciences; 1.108 Molecular & Cell Biology - Cancer & Development; 1.108.207 Neural Crest
Web Of Science research areas: Biochemistry & Molecular Biology; Biophysics
ESI research areas: Biology & Biochemistry

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Details

Title: Deficient Alk3-mediated BMP signaling causes prenatal omphalocele-like defect
Creators: Jianping Sun - Developmental Biology Program, Department of Surgery, Childrens Hospital Los Angeles, 4650 Sunset Boulevard, MS 35, Los Angeles, CA 90027, USA
Yi-Hsin Liu - Department of Ophthalmology, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA
Hui Chen - Developmental Biology Program, Department of Surgery, Childrens Hospital Los Angeles, 4650 Sunset Boulevard, MS 35, Los Angeles, CA 90027, USA
Manuel P Nguyen - Department of Ophthalmology, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA
Yuji Mishina - Molecular Developmental Biology Group, Laboratory of Reproductive and Developmental Toxicology, National Institutes of Health, Research Triangle Park, NC 27709, USA
Jeffrey S Upperman - Developmental Biology Program, Department of Surgery, Childrens Hospital Los Angeles, 4650 Sunset Boulevard, MS 35, Los Angeles, CA 90027, USA
Henri R Ford - Developmental Biology Program, Department of Surgery, Childrens Hospital Los Angeles, 4650 Sunset Boulevard, MS 35, Los Angeles, CA 90027, USA
Wei Shi - Developmental Biology Program, Department of Surgery, Childrens Hospital Los Angeles, 4650 Sunset Boulevard, MS 35, Los Angeles, CA 90027, USA
Publication Details: Biochemical and biophysical research communications, Vol.360(1), pp.238-243
Publisher: Elsevier Inc
Academic Unit: Health Affairs Administration; Health Affairs Administration; Leadership Department
Language: English
Resource Type: Journal article
PMID: 17588538
PMCID: PMC1987715
Record Identifier: 991031613437702976