期刊
NATURE STRUCTURAL & MOLECULAR BIOLOGY
卷 18, 期 6, 页码 665-U60出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/nsmb.2049
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资金
- US National Institutes of Health, National Eye Institute [RO1 EY14597]
- Natural Sciences and Engineering Research Council of Canada [RGPIN/203545]
- Canadian Institutes of Health Research [MOP 62895]
- US National Institutes of Health [GM076561]
Frizzled planar cell polarity (PCP) signaling regulates cell motility in several tissues, including ommatidial rotation in Drosophila melanogaster. The Nemo kinase (Nlk in vertebrates) has also been linked to cell-motility regulation and ommatidial rotation but its mechanistic role(s) during rotation remain obscure. We show that nemo functions throughout the entire rotation movement, increasing the rotation rate. Genetic and molecular studies indicate that Nemo binds both the core PCP factor complex of Strabismus-Prickle, as well as the E-cadherin-beta-catenin (E-cadherin-Armadillo in Drosophila) complex. These two complexes colocalize and, like Nemo, also promote rotation. Strabismus (also called Vang) binds and stabilizes Nemo asymmetrically within the ommatidial precluster; Nemo and beta-catenin then act synergistically to promote rotation, which is mediated in vivo by Nemo's phosphorylation of beta-catenin. Our data suggest that Nemo serves as a conserved molecular link between core PCP factors and E-cadherin-beta-catenin complexes, promoting cell motility.
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