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Fzd3 and Fzd6 play a redundant role in controlling the polarity of developing skin, but through non-identical mechanisms.
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The authors report here that Sonic Hedgehog (Shh)-Smoothened signaling downregulates Shisa2, which inhibits the glycosylation and cell surface presentation of Frizzled3 in rodent commissural axon growth cones.
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Results suggest that Celsr3 and Fzd3 orchestrate the formation of a scaffold of pioneer neurons and their axons during embryogenesis. This scaffold extends from prethalamus to ventral telencephalon and subcortex, and steers reciprocal corticothalamic fibers.
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Frizzled3 is required to shape the pattern of RBC somas and dendrites, and the structural and functional connectivity between rods and RBCs. Our results highlight novel functions for Fzd3 in regulating retinal development.
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Temporal and spatial expression profiles of Frizzled 3 in the ovary during the estrous cycle has been reported.
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Celsr3 and Fzd3 enable immature neurons to respond to Wnt7, upregulate Jag1 and thereby facilitate feedback signals that tune the timing of neural progenitor cell fate decisions via Notch activation.
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This study demonstrated that Frizzled3 Controls Axonal Polarity and Intermediate Target Entry during Striatal Pathway Development.
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In Fz3(-/-) limbs, dorsal axons stall at a precise location in the nerve plexus, and, in contrast to the phenotypes of several other axon path-finding mutants, Fz3(-/-) dorsal axons do not reroute to other trajectories
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Wnt3a/Frizzled-3 signaling plays important role in regulating the proliferation and differentiation of neural crest cells and various developmental stages of melanocyte precursors.
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Fz3 and Fz6 have partly interchangeable roles in tissue polarity signaling for epithelial orientation and axon growth and guidance
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The first signal, controlled by cadherin, EGF-like, laminin G-like, seven-pass, G-type receptor (Celsr) 2, Celsr3, Frizzled3 (Fzd3) and Van Gogh like2 (Vangl2) organizes multicilia in individual cells (single-cell polarity)
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Celsr2-3 and Fzd3 regulate axonal navigation in the forebrain by using mechanisms different from classical epithelial core planar cell polarity, and require interacting partners other than Vangl1-2 that remain to be identified.
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Several central nervous system axon tracts require Fz3 function as early as embryonic day 11.5, and that Fz3 is required for pathfinding by dopaminergic and serotonergic axons in the brain and by a subset of optic tract axons.
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Frizzled3 endocytosis is part of the key mechanism for growth cone steering
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Celsr3 and Fzd3 are required during murine embryogenesis to specifically control the guidance and growth of enteric neuronal projections relative to the longitudinal and radial gut axes.
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The results of this study suggested distinct roles for Fz3 during sympathetic neuron development; Fz3 acts at early developmental stages to maintain a pool of dividing sympathetic precursors.
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Fzd3 and Fzd6 deficiency results in a severe midbrain morphogenesis defect.
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commissural axons in mice lacking the Wnt receptor Frizzled3 displayed anterior-posterior guidance defects after midline crossing; Wnt-Frizzled signaling guides commissural axons along the anterior-posterior axis of the spinal cord
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In the inner ear of a Vangl2 mutant (Looptail; Lp), Fz3 and Fz6 proteins accumulate to normal levels but do not localize correctly at the cell surface.
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Together, our data support the idea that protein asymmetry plays an important role in the development of PCP, but the colocalization and interaction of Fz3 and Vangl2 suggests that novel PCP mechanisms exist in vertebrates.
