| Disheveled mediated planar cell polarity signaling is required in the second heart field lineage for outflow tract morphogenesis. | |
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MedLine Citation:
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PMID: 22841628 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Disheveled (Dvl) is a key regulator of both the canonical Wnt and the planar cell polarity (PCP) pathway. Previous genetic studies in mice indicated that outflow tract (OFT) formation requires Dvl1 and 2, but it was unclear which pathway was involved and whether Dvl1/2-mediated signaling was required in the second heart field (SHF) or the cardiac neural crest (CNC) lineage, both of which are critical for OFT development. In this study, we used Dvl1/2 null mice and a set of Dvl2 BAC transgenes that function in a pathway-specific fashion to demonstrate that Dvl1/2-mediated PCP signaling is essential for OFT formation. Lineage-specific gene-ablation further indicated that Dvl1/2 function is dispensable in the CNC, but required in the SHF for OFT lengthening to promote cardiac looping. Mutating the core PCP gene Vangl2 and non-canonical Wnt gene Wnt5a recapitulated the OFT morphogenesis defects observed in Dvl1/2 mutants. Consistent with genetic interaction studies suggesting that Wnt5a signals through the PCP pathway, Dvl1/2 and Wnt5a mutants display aberrant cell packing and defective actin polymerization and filopodia formation specifically in SHF cells in the caudal splanchnic mesoderm (SpM), where Wnt5a and Dvl2 are co-expressed specifically. Our results reveal a critical role of PCP signaling in the SHF during early OFT lengthening and cardiac looping and suggest that a Wnt5a→ Dvl PCP signaling cascade may regulate actin polymerization and protrusive cell behavior in the caudal SpM to promote SHF deployment, OFT lengthening and cardiac looping. |
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Authors:
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Tanvi Sinha; Bing Wang; Sylvia Evans; Anthony Wynshaw-Boris; Jianbo Wang |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't Date: 2012-07-27 |
Journal Detail:
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Title: Developmental biology Volume: 370 ISSN: 1095-564X ISO Abbreviation: Dev. Biol. Publication Date: 2012 Oct |
Date Detail:
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Created Date: 2012-09-03 Completed Date: 2012-11-08 Revised Date: 2013-04-16 |
Medline Journal Info:
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Nlm Unique ID: 0372762 Medline TA: Dev Biol Country: United States |
Other Details:
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Languages: eng Pagination: 135-44 Citation Subset: IM |
Copyright Information:
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Copyright © 2012 Elsevier Inc. All rights reserved. |
Affiliation:
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Department of Cell, Developmental and Integrative Biology, University of Alabama at Birmingham, 1918 University Blvd., Birmingham, AL 35294, UK. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Actins
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metabolism* Adaptor Proteins, Signal Transducing / deficiency, metabolism* Animals Cell Polarity / physiology* Chromosomes, Artificial, Bacterial / genetics DNA Primers / genetics Heart / embryology* Immunohistochemistry In Situ Hybridization Mice Morphogenesis / genetics, physiology* Mutagenesis Nerve Tissue Proteins / genetics Phosphoproteins / deficiency, metabolism* Polymerization Real-Time Polymerase Chain Reaction Signal Transduction / physiology* Transgenes / genetics Wnt Proteins / genetics |
| Grant Support | |
ID/Acronym/Agency:
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R01 HL109130/HL/NHLBI NIH HHS; R01HL109130/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Actins; 0/Adaptor Proteins, Signal Transducing; 0/DNA Primers; 0/Ltap protein, mouse; 0/Nerve Tissue Proteins; 0/Phosphoproteins; 0/Wnt Proteins; 0/Wnt5a protein, mouse; 0/dishevelled proteins |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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