Frizzled3a and Celsr2 function in the neuroepithelium to regulate migration of facial motor neurons in the developing zebrafish hindbrain

Wada, Hironori; Tanaka, Hideomi; Nakayama, Shidai; Iwasaki, Miki; Okamoto, Hitoshi

doi:10.1242/dev.02665

Cited by 110 publications

(216 citation statements)

References 47 publications

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“…This is in contrast to results with other PCP components and is inconsistent with the prevailing model of PCP interactions (for reviews, see Klein and Mlodzik, 2005;Wang and Nathans, 2007): the expression and localization of core PCP proteins are tightly regulated among cells, such that reductions or elevations of protein levels result in the same mispolarization phenotype. Third, transplantation experiments indicate that Pk1b functions primarily cell-autonomously within FBMNs (Rohrschneider et al, 2007), whereas other PCP components function primarily non-cell-autonomously (Jessen et al, 2002;Wada et al, 2006). Together, these observations suggest that Pk1b might function independently of other PCP components.…”

Section: Introductionmentioning

confidence: 82%

“…Among many proteins known to regulate this migration in zebrafish are several core planar cell polarity (PCP) components (reviewed by Wada and Okamoto, 2009a;Wada and Okamoto, 2009b). These molecules include Vang-like 2 (Vangl2) (Jessen et al, 2002;Bingham et al, 2002); Frizzled 3a (Fzd3a), Cadherin EGF LAG seven-pass G-type receptor 1a (Celsr1a), Celsr1b, Celsr2 (Wada et al, 2006); Scribble 1 (Scrib) (Wada et al, 2005); Prickle1a (Pk1a) (Carreira-Barbosa et al, 2003); and Pk1b (Rohrschneider et al, 2007). Several characteristics of Pk1b make it unique among these PCP components.…”

Section: Introductionmentioning

confidence: 99%

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Zebrafish Prickle1b mediates facial branchiomotor neuron migration via a farnesylation-dependent nuclear activity

et al. 2011

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SUMMARYThe facial branchiomotor neurons (FBMNs) undergo a characteristic tangential migration in the vertebrate hindbrain. We previously used a morpholino knockdown approach to reveal that zebrafish prickle1b (pk1b) is required for this migration. Here we report that FBMN migration is also blocked in a pk1b mutant with a disruption in the consensus farnesylation motif. We confirmed that this lipid modification is required during FBMN migration by disrupting the function of farnesyl biosynthetic enzymes. Furthermore, farnesylation of a tagged Pk1b is required for its nuclear localization. Using a unique rescue approach, we have demonstrated that Pk1b nuclear localization and farnesylation are required during FBMN migration. Our data suggest that Pk1b acts at least partially independently of core planar cell polarity molecules at the plasma membrane, and might instead be acting at the nucleus. We also found that the neuronal transcriptional silencer REST is necessary for FBMN migration, and we provide evidence that interaction between Pk1b and REST is required during this process. Finally, we demonstrate that REST protein, which is normally localized in the nuclei of migrating FBMNs, is depleted from the nuclei of Pk1b-deficient neurons. We conclude that farnesylation-dependent nuclear localization of Pk1b is required to regulate REST localization and thus FBMN migration.

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Section: Introductionmentioning

confidence: 82%

Section: Introductionmentioning

confidence: 99%

Zebrafish Prickle1b mediates facial branchiomotor neuron migration via a farnesylation-dependent nuclear activity

et al. 2011

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“…In many cases the identity of the Wnt ligand is not clear since only Wnt signaling (Houart et al, 2002;Kapsimali et al, 2004;Yu et al, 2008;Joksimovic et al, 2009;) or the Frizzled receptor (Wang et al, 2002;Wada et al, 2006;Wang et al, 2006a;Wang et al, 2006b) has been investigated.…”

Section: Discussionmentioning

confidence: 99%

“…Loss of function studies in mouse and fish have linked Fzd3 to the planar cell polarity pathway (Wang et al, 2002;Lyuksyutova et al, 2003;Wada et al, 2006;Wang et al, 2006a;Wang et al, 2006b). In vitro studies indicate that mFzd3 can cause an increase in intracellular Ca 2+ levels (Slusarski et al, 1997a;Slusarski et al, 1997b;Liu et al, 1999;Kuhl et al, 2000;Sheldahl et al, 2003;), thereby implicating the Wnt/Ca 2+ signaling pathway.…”

Section: Discussionmentioning

confidence: 99%

Frizzled-3a and Wnt-8b genetically interact during forebrain commissural formation in embryonic zebrafish

Hofmeister

Key

2013

Brain Research

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Number of words: 3225Key words: Wnt8b, Fzd3a, axon guidance, commissure, zebrafish, slit2Keyfindings:• Knockdown of Wnt8b results in an absence of the anterior commissure and a reduction of the post-optic commissure • Knockdown of Wnt8b results in a expansion of slit2 at the rostral midline and a reduction of the glial bridge • The phenotype observed following knockdown of Wnt8b is similar to that seen following knockdown of Fzd3a • Combined loss of both Wnt8b and Fzd3a caused a synergistic increase in commissural defects and abnormal slit2 expression • Fzd3a and Wnt8b act in the same genetic pathway to control normal patterning of the commissural plate Acknowledgements: This work was supported by grants from NHMRC and ARC to B.K.2 AbstractThe commissural plate forms the rostral surface of the embryonic vertebrate forebrain and provides a cellular substrate for forebrain commissural axons. We have previously reported that the Wnt receptor frizzled-3a (fzd3a) restricts the expression of the chemorepulsive guidance ligand slit2 to a discrete domain of neuroepithelial cells in the commissural plate of embryonic zebrafish. Loss-of-Fzd3a function perturbed slit2 expression and disrupted the formation of glial bridges which guide the formation of forebrain commissures. We now show that Wnt8b is also necessary for anterior commissural formation as well as for patterning of slit2 expression at the midline. Knock down of Wnt8b produced the same phenotype as loss of Fzd3a which suggested that these genes were acting together to regulate axon guidance. Simultaneous sub-threshold knock down of both Fzd3a and Wnt8b led to a greater than additive increase in the penetrance of the mutant phenotype which indicated that these two genes were indeed interacting. We have shown here that Fzd3a/Wnt8b signaling is essential for normal patterning of the commissural plate and that loss-of-function in either receptor or ligand causes Slit2-dependent defects in glial bridge morphology which indirectly attenuated axon midline crossing in the embryonic vertebrate forebrain.3

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“…Furthermore, the migration of facial branchiomotor (FBM) neurons [24][25][26][27][28][29][30][31] and neural crest cells [32] depends on the function of the PCP genes, as does neuronal morphogenesis in the postnatal hippocampus [33,34] and OB [35], indicating that PCP signaling is involved in the migration and differentiation of many types of neural cells [36][37][38]. However, the function of this signaling pathway in the postnatal migration and differentiation of neurons in the OB has not been clearly demonstrated.…”

Section: Introductionmentioning

confidence: 99%

Roles of Planar Cell Polarity Signaling in Maturation of Neuronal Precursor Cells in the Postnatal Mouse Olfactory Bulb

et al. 2012

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Neuronal precursor cells generated by stem cells in the subventricular zone (SVZ) migrate and differentiate into mature interneurons in the olfactory bulb (OB). The mechanisms responsible for the dynamic morphological changes in cells during this process are largely unknown. Wnt/planar cell polarity (PCP) signaling regulates various developmental events, including neuronal migration and neurite formation. Here, we studied the function of two components of the PCP pathway, Dishevelled2 and Van Gogh like-2, in the newborn neurons in the postnatal mouse OB. Electroporation-or lentivirus-mediated introduction of vectors carrying a knockdown or dominant-negative construct of these genes into the SVZ altered the distribution and dendrite formation of newborn neurons in the OB, suggesting that PCP signaling is involved in regulating the maturation of new neurons in the OB.

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Frizzled3a and Celsr2 function in the neuroepithelium to regulate migration of facial motor neurons in the developing zebrafish hindbrain

Cited by 110 publications

References 47 publications

Zebrafish Prickle1b mediates facial branchiomotor neuron migration via a farnesylation-dependent nuclear activity

Zebrafish Prickle1b mediates facial branchiomotor neuron migration via a farnesylation-dependent nuclear activity

Frizzled-3a and Wnt-8b genetically interact during forebrain commissural formation in embryonic zebrafish

Roles of Planar Cell Polarity Signaling in Maturation of Neuronal Precursor Cells in the Postnatal Mouse Olfactory Bulb

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