Structural and temporal requirements of Wnt/PCP protein Vangl2 function for convergence and extension movements and facial branchiomotor neuron migration in zebrafish

Pan, Xiufang; Sittaramane, Vinoth; Gurung, Suman; Chandrasekhar, Anand

doi:10.1016/j.mod.2013.12.001

Cited by 15 publications

(13 citation statements)

References 71 publications

(104 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Elimination of one guidance mechanism, such as Cdh2 neuron-to-neuron interactions, severely limits the overall effectiveness of caudal migration. Interestingly, partial migration phenotypes and ‘escaper’ neurons are not observed in embryos with mutations in PCP components[ 16 , 18 – 21 , 41 ], in which FBMNs completely fail to exit r4, despite the observation that PCP mutant FBMNs are motile and migrate randomly within r4 [ 19 , 40 ]. This suggests that Cdh2-deficient FBMNs may rely on PCP-dependent migration to undergo limited and sparing migration out of r4.…”

Section: Discussionmentioning

confidence: 99%

Cadherin-2 Is Required Cell Autonomously for Collective Migration of Facial Branchiomotor Neurons

2016

View full text Add to dashboard Cite

Collective migration depends on cell-cell interactions between neighbors that contribute to their overall directionality, yet the mechanisms that control the coordinated migration of neurons remains to be elucidated. During hindbrain development, facial branchiomotor neurons (FBMNs) undergo a stereotypic tangential caudal migration from their place of birth in rhombomere (r)4 to their final location in r6/7. FBMNs engage in collective cell migration that depends on neuron-to-neuron interactions to facilitate caudal directionality. Here, we demonstrate that Cadherin-2-mediated neuron-to-neuron adhesion is necessary for directional and collective migration of FBMNs. We generated stable transgenic zebrafish expressing dominant-negative Cadherin-2 (Cdh2ΔEC) driven by the islet1 promoter. Cell-autonomous inactivation of Cadherin-2 function led to non-directional migration of FBMNs and a defect in caudal tangential migration. Additionally, mosaic analysis revealed that Cdh2ΔEC-expressing FBMNs are not influenced to migrate caudally by neighboring wild-type FBMNs due to a defect in collective cell migration. Taken together, our data suggest that Cadherin-2 plays an essential cell-autonomous role in mediating the collective migration of FBMNs.

show abstract

Section: Discussionmentioning

confidence: 99%

Cadherin-2 Is Required Cell Autonomously for Collective Migration of Facial Branchiomotor Neurons

2016

View full text Add to dashboard Cite

show abstract

“…Thus, the role of this atypical cadherin is different to the role of classical type II cadherins including Cadherin 11 (Borchers et al, 2001;Kashef et al, 2009) and also different to the protocadherin PAPC (Schneider et al, 2010). Instead, Vangl proteins have been shown to be essential for planar cell polarity (PCP) in Drosophila (Jenny et al, 2003), zebrafish (Pan et al, 2014) and mouse (Pryor et al, 2014). Vangl2 is essential for neural crest migration in Xenopus and zebrafish Matthews et al, 2008) and regulates cell polarity and cell motility in Xenopus (Borchers et al, 2001).…”

Section: Discussionmentioning

confidence: 99%

Neural crest specification by Prohibitin1 depends on transcriptional regulation of prl3 and vangl1

Deichmann¹,

Link²,

Seyfang³

et al. 2015

Genesis

View full text Add to dashboard Cite

A complex network of transcription factors regulates specification of neural crest cells at early neurula stage by stabilizing neural crest identity and activating neural crest effector genes so that distinct subpopulations evolve. In this network, c-myc acts on top of the gene hierarchy controlling snail2, AP2 and prohibitin1 (phb1) expression. While snail2 and AP2 are well studied neural crest specifier genes little is known about the role of phb1 in this process. To identify phb1 regulated genes we analyzed the transcriptome of neural crest explants of phb1 morphant Xenopus embryos. Among 147 phb1 regulated genes we identified the membrane-associated protein-tyrosine phosphatase PRP4A3 (prl3) and the atypical cadherin and Wnt-PCP component van gogh like1 (vangl1). Gain of function, loss of function and epistasis experiments allowed us to allocate both genes in the neural crest specification network between phb1 and twist. Interestingly, both, vangl1 and prl3 regulate only a small subset of neural crest marker genes. The identification of two membrane-associated proteins as novel neural crest specifiers indicates that in addition to gene regulation by combinatory effects of transcription factors also post-translational modifications (prl3) and cell-cell adhesion and/or regulation of cell-polarity (vangl1) specify the identity of neural crest cell populations. genesis 53:627-639, 2015. © 2015 Wiley Periodicals, Inc.

show abstract

“…We tested this possibility by creating a transgenic zebrafish expressing human HCFC1 under the control of the heat shock promoter for the hsp701 gene. The efficacy of the hsp701 promoter in zebrafish has been widely established in previous studies (28,(39)(40)(41)(42)(43). We activated expression of HCFC1 by performing a heat shock as described in the methods section for a period of 5 days.…”

Section: Overexpression Of Hcfc1 Reduces the Number Of Npcs And Decrementioning

confidence: 99%

Hcfc1a regulates neural precursor proliferation and asxl1 expression in the developing brain.

Castro

Reyes

Reyes-Nava

et al. 2020

Preprint

View full text Add to dashboard Cite

Background: Precise regulation of neural precursor cell (NPC) proliferation and differentiation is essential to ensure proper brain development and function. The HCFC1 gene encodes a transcriptional co-factor that regulates cell proliferation, and previous studies suggest that HCFC1 regulates NPC function. However, the molecular mechanism underlying these cellular deficits has not been completely characterized. Methods: Here we created a zebrafish harboring mutations in the hcfc1a gene (the hcfc1a co60/+ allele), one ortholog of HCFC1 and utilized immunohistochemistry and RNA-sequencing technology to understand the function of hcfc1a during neural development. Results: The hcfc1a co60/+ allele results in an increased number of NPCs, neurons, and radial glial cells. These deficits are associated with the abnormal expression of asxl1 , a polycomb transcription factor, which we identified as a downstream effector of hcfc1a using high throughput RNA sequencing technology. Inhibition of asxl1 activity and/or expression in larvae harboring the hcfc1a co60/+ allele completely restored the number of NPCs to normal levels. Conclusion: Collectively, our data demonstrate a novel pathway in which hcfc1a regulates NPCs and neurogenesis.

show abstract

Structural and temporal requirements of Wnt/PCP protein Vangl2 function for convergence and extension movements and facial branchiomotor neuron migration in zebrafish

Cited by 15 publications

References 71 publications

Cadherin-2 Is Required Cell Autonomously for Collective Migration of Facial Branchiomotor Neurons

Cadherin-2 Is Required Cell Autonomously for Collective Migration of Facial Branchiomotor Neurons

Neural crest specification by Prohibitin1 depends on transcriptional regulation of prl3 and vangl1

Hcfc1a regulates neural precursor proliferation and asxl1 expression in the developing brain.

Contact Info

Product

Resources

About