1. Planar cell polarity breaks bilateral symmetry by controlling ciliary positioning
- Author
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Song, Hai, Hu, Jianxin, Chen, Wen, Elliott, Gene, Andre, Philipp, Gao, Bo, and Yang, Yingzi
- Subjects
Biological research -- Research -- Physiological aspects ,Biology, Experimental -- Research -- Physiological aspects ,Cilia and ciliary motion -- Physiological aspects -- Research ,Polarity (Biology) -- Research -- Physiological aspects ,Environmental issues ,Science and technology ,Zoology and wildlife conservation - Abstract
Body line decisions The three animal body axes are established sequentially during development -- first the anteroposterior and dorsoventral axes, and then left-right asymmetry -- but how the latter derives from the former has been unclear. Now, Yingzi Yang and colleagues show that two mouse genes belonging to the 'planar cell polarity' family (Vangl1 and Vangl2) are required for the posterior deposition of cilia, which in turn determines the leftward nodal flow across the posterior notochord. This work suggests that planar cell polarity is an evolutionarily conserved mechanism that transmits the predetermined anteroposterior positional information and converts it to the first lateral symmetry-breaking event in the embryo. During vertebrate development, the dorsal-ventral and anterior-posterior (A-P) body axes are determined first, after which left-right (L-R) asymmetry is established. But the molecular mechanism by which L-R symmetry is broken in reference to the other two axes is poorly understood. Here it is shown that two mouse genes, Vang1 and Vang2, which belong to the planar cell polarity family, are required to interpret the A-P patterning information and link it to L-R asymmetry. Defining the three body axes is a central event of vertebrate morphogenesis. Establishment of left-right (L-R) asymmetry in development follows the determination of dorsal-ventral and anterior-posterior (A-P) body axes.sup.1,2, although the molecular mechanism underlying precise L-R symmetry breaking in reference to the other two axes is still poorly understood. Here, by removing both Vangl1 and Vangl2, the two mouse homologues of a Drosophila core planar cell polarity (PCP) gene Van Gogh (Vang), we reveal a previously unrecognized function of PCP in the initial breaking of lateral symmetry. The leftward nodal flow across the posterior notochord (PNC) has been identified as the earliest event in the de novo formation of L-R asymmetry.sup.3,4. We show that PCP is essential in interpreting the A-P patterning information and linking it to L-R asymmetry. In the absence of Vangl1 and Vangl2, cilia are positioned randomly around the centre of the PNC cells and nodal flow is turbulent, which results in disrupted L-R asymmetry. PCP in mouse, unlike what has been implicated in other vertebrate species, is not required for ciliogenesis, cilium motility, Sonic hedgehog (Shh) signalling or apical docking of basal bodies in ciliated tracheal epithelial cells. Our data suggest that PCP acts earlier than the unidirectional nodal flow during bilateral symmetry breaking in vertebrates and provide insight into the functional mechanism of PCP in organizing the vertebrate tissues in development., Author(s): Hai Song [sup.1] , Jianxin Hu [sup.1] , Wen Chen [sup.1] , Gene Elliott [sup.2] , Philipp Andre [sup.1] , Bo Gao [sup.1] , Yingzi Yang [sup.1] Author Affiliations: [...]
- Published
- 2010
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