Document Detail


Chongmague reveals an essential role for laminin-mediated boundary formation in chordate convergence and extension movements.
MedLine Citation:
PMID:  18032448     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Although cell intercalation driven by non-canonical Wnt/planar cell polarity (PCP) pathway-dependent mediolateral cell polarity is important for notochord morphogenesis, it is likely that multiple mechanisms shape the notochord as it converges and extends. Here we show that the recessive short-tailed Ciona savignyi mutation chongmague (chm) has a novel defect in the formation of a morphological boundary around the developing notochord. chm notochord cells initiate intercalation normally, but then fail to maintain their polarized cell morphology and migrate inappropriately to become dispersed in the larval tail. This is unlike aimless (aim), a mutation in the PCP pathway component Prickle, which has a severe defect in early mediolateral intercalation but forms a robust notochord boundary. Positional cloning identifies chm as a mutation in the C. savignyi ortholog of the vertebrate alpha 3/4/5 family of laminins. Cs-lamalpha3/4/5 is highly expressed in the developing notochord, and Cs-lamalpha3/4/5 protein is specifically localized to the outer border of the notochord. Notochord convergence and extension, reduced but not absent in both chm and aim, are essentially abolished in the aim/aim; chm/chm double mutant, indicating that laminin-mediated boundary formation and PCP-dependent mediolateral intercalation are each able to drive a remarkable degree of tail morphogenesis in the absence of the other. These mechanisms therefore initially act in parallel, but we also find that PCP signaling has an important later role in maintaining the perinotochordal/intranotochordal polarity of Cs-lamalpha3/4/5 localization.
Authors:
Michael T Veeman; Yuki Nakatani; Carolyn Hendrickson; Vivian Ericson; Clarissa Lin; William C Smith
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2007-11-21
Journal Detail:
Title:  Development (Cambridge, England)     Volume:  135     ISSN:  0950-1991     ISO Abbreviation:  Development     Publication Date:  2008 Jan 
Date Detail:
Created Date:  2007-12-10     Completed Date:  2008-03-04     Revised Date:  2011-06-01    
Medline Journal Info:
Nlm Unique ID:  8701744     Medline TA:  Development     Country:  England    
Other Details:
Languages:  eng     Pagination:  33-41     Citation Subset:  IM    
Affiliation:
Department of Molecular, Cell and Developmental Biology, University of California Santa Barbara, Santa Barbara CA, 93106, USA.
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MeSH Terms
Descriptor/Qualifier:
Amino Acid Sequence
Animals
Apoptosis
Base Sequence
Cell Polarity
Cell Shape
Chordata / embryology*,  metabolism*
Embryo, Nonmammalian / cytology,  embryology,  metabolism
Gene Expression Regulation, Developmental
Laminin / chemistry,  genetics,  metabolism*
Molecular Sequence Data
Mutation / genetics
Signal Transduction
Time Factors
Urochordata / cytology,  embryology,  metabolism*
Wnt Proteins / metabolism
Grant Support
ID/Acronym/Agency:
GM075049/GM/NIGMS NIH HHS; HD038701/HD/NICHD NIH HHS; R01 HD038701-08/HD/NICHD NIH HHS
Chemical
Reg. No./Substance:
0/Laminin; 0/Wnt Proteins
Comments/Corrections

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