| Two populations of node monocilia initiate left-right asymmetry in the mouse. | |
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MedLine Citation:
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PMID: 12859898 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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The vertebrate body plan has conserved handed left-right (LR) asymmetry that is manifested in the heart, lungs, and gut. Leftward flow of extracellular fluid at the node (nodal flow) is critical for normal LR axis determination in the mouse. Nodal flow is generated by motile node cell monocilia and requires the axonemal dynein, left-right dynein (lrd). In the absence of lrd, LR determination becomes random. The cation channel polycystin-2 is also required to establish LR asymmetry. We show that lrd localizes to a centrally located subset of node monocilia, while polycystin-2 is found in all node monocilia. Asymmetric calcium signaling appears at the left margin of the node coincident with nodal flow. These observations suggest that LR asymmetry is established by an entirely ciliary mechanism: motile, lrd-containing monocilia generate nodal flow, and nonmotile polycystin-2 containing cilia sense nodal flow initiating an asymmetric calcium signal at the left border of the node. |
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Authors:
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James McGrath; Stefan Somlo; Svetlana Makova; Xin Tian; Martina Brueckner |
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Publication Detail:
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Type: Journal Article; Research Support, U.S. Gov't, P.H.S. |
Journal Detail:
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Title: Cell Volume: 114 ISSN: 0092-8674 ISO Abbreviation: Cell Publication Date: 2003 Jul |
Date Detail:
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Created Date: 2003-07-15 Completed Date: 2003-08-13 Revised Date: 2009-11-19 |
Medline Journal Info:
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Nlm Unique ID: 0413066 Medline TA: Cell Country: United States |
Other Details:
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Languages: eng Pagination: 61-73 Citation Subset: IM |
Affiliation:
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Department of Comparative Medicine, Yale University School of Medicine, New Haven, CT 06520, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Axonemal Dyneins Body Patterning / physiology* Calcium Signaling / physiology Cilia / metabolism*, ultrastructure Dyneins / deficiency, genetics Epithelial Cells / cytology, metabolism Extracellular Space / metabolism* Female Fetus Functional Laterality / physiology* Gastrula / cytology, metabolism* Membrane Proteins / deficiency, genetics Mice Mice, Knockout Mutation / genetics Organizers, Embryonic / cytology, embryology*, metabolism Pregnancy Recombinant Fusion Proteins / diagnostic use TRPP Cation Channels |
| Grant Support | |
ID/Acronym/Agency:
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DK54053/DK/NIDDK NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Dnahc11 protein, mouse; 0/Membrane Proteins; 0/Recombinant Fusion Proteins; 0/TRPP Cation Channels; 0/polycystic kidney disease 2 protein; EC 3.6.4.2/Axonemal Dyneins; EC 3.6.4.2/Dyneins |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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