Hdl Handle:
http://hdl.handle.net/10675.2/784
Title:
Wnt proteins regulate acetylcholine receptor clustering in muscle cells
Authors:
Zhang, Bin; Liang, Chuan; Bates, Ryan; Yin, Yiming; Xiong, Wen-Cheng; Mei, Lin
Abstract:
Background: The neuromuscular junction (NMJ) is a cholinergic synapse that rapidly conveys signals from motoneurons to muscle cells and exhibits a high degree of subcellular specialization characteristic of chemical synapses. NMJ formation requires agrin and its coreceptors LRP4 and MuSK. Increasing evidence indicates that Wnt signaling regulates NMJ formation in Drosophila, C. elegans and zebrafish.; Results: In the study we systematically studied the effect of all 19 different Wnts in mammals on acetylcholine receptor (AChR) cluster formation. We identified five Wnts (Wnt9a, Wnt9b, Wnt10b, Wnt11, and Wnt16) that are able to stimulate AChR clustering, of which Wnt9a and Wnt11 are expressed abundantly in developing muscles. Using Wnt9a and Wnt11 as example, we demonstrated that Wnt induction of AChR clusters was dose-dependent and non-additive to that of agrin, suggesting that Wnts may act via similar pathways to induce AChR clusters. We provide evidence that Wnt9a and Wnt11 bind directly to the extracellular domain of MuSK, to induce MuSK dimerization and subsequent tyrosine phosphorylation of the kinase. In addition, Wnt-induced AChR clustering requires LRP4.; Conclusions: These results identify Wnts as new players in AChR cluster formation, which act in a manner that requires both MuSK and LRP4, revealing a novel function of LRP4.
Citation:
Mol Brain. 2012 Feb 6; 5:7
Issue Date:
6-Feb-2012
URI:
http://hdl.handle.net/10675.2/784
DOI:
10.1186/1756-6606-5-7
PubMed ID:
22309736
PubMed Central ID:
PMC3296622
Type:
Article
ISSN:
1756-6606
Appears in Collections:
Department of Neurology: Faculty Research and Presentations

Full metadata record

DC FieldValue Language
dc.contributor.authorZhang, Binen_US
dc.contributor.authorLiang, Chuanen_US
dc.contributor.authorBates, Ryanen_US
dc.contributor.authorYin, Yimingen_US
dc.contributor.authorXiong, Wen-Chengen_US
dc.contributor.authorMei, Linen_US
dc.date.accessioned2012-10-26T20:30:44Z-
dc.date.available2012-10-26T20:30:44Z-
dc.date.issued2012-02-6en_US
dc.identifier.citationMol Brain. 2012 Feb 6; 5:7en_US
dc.identifier.issn1756-6606en_US
dc.identifier.pmid22309736en_US
dc.identifier.doi10.1186/1756-6606-5-7en_US
dc.identifier.urihttp://hdl.handle.net/10675.2/784-
dc.description.abstractBackground: The neuromuscular junction (NMJ) is a cholinergic synapse that rapidly conveys signals from motoneurons to muscle cells and exhibits a high degree of subcellular specialization characteristic of chemical synapses. NMJ formation requires agrin and its coreceptors LRP4 and MuSK. Increasing evidence indicates that Wnt signaling regulates NMJ formation in Drosophila, C. elegans and zebrafish.en_US
dc.description.abstractResults: In the study we systematically studied the effect of all 19 different Wnts in mammals on acetylcholine receptor (AChR) cluster formation. We identified five Wnts (Wnt9a, Wnt9b, Wnt10b, Wnt11, and Wnt16) that are able to stimulate AChR clustering, of which Wnt9a and Wnt11 are expressed abundantly in developing muscles. Using Wnt9a and Wnt11 as example, we demonstrated that Wnt induction of AChR clusters was dose-dependent and non-additive to that of agrin, suggesting that Wnts may act via similar pathways to induce AChR clusters. We provide evidence that Wnt9a and Wnt11 bind directly to the extracellular domain of MuSK, to induce MuSK dimerization and subsequent tyrosine phosphorylation of the kinase. In addition, Wnt-induced AChR clustering requires LRP4.en_US
dc.description.abstractConclusions: These results identify Wnts as new players in AChR cluster formation, which act in a manner that requires both MuSK and LRP4, revealing a novel function of LRP4.en_US
dc.rightsCopyright ©2012 Zhang et al; licensee BioMed Central Ltd.en_US
dc.titleWnt proteins regulate acetylcholine receptor clustering in muscle cellsen_US
dc.typeArticleen_US
dc.identifier.pmcidPMC3296622en_US
dc.contributor.corporatenameDepartment of Neurology-
dc.contributor.corporatenameInstitute of Molecular Medicine and Genetics-

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