Zebrafish Wnt9a,9b paralog comparisons suggest ancestral roles for Wnt9 in neural, oral–pharyngeal ectoderm and mesendoderm

Cox, A.A.; Jezewski, Peter A.; Fang, Ping-Ke; Payne-Ferreira, Tracie L.

doi:10.1016/j.gep.2010.05.005

Cited by 12 publications

(15 citation statements)

References 29 publications

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“…The Wnt9 genes have been recognized as critically important in the ancestral patterning of ectodermal and mesoendodermal morphogenesis (7). These effects of carrageenan, on stimulation of both Wnt9A expression and Wnt/␤-catenin signaling, demonstrate the profound influence of a common dietary component on a major pathway of colon carcinogenesis.…”

mentioning

confidence: 99%

Increased Expression of Colonic Wnt9A through Sp1-mediated Transcriptional Effects involving Arylsulfatase B, Chondroitin 4-Sulfate, and Galectin-3

Bhattacharyya

Feferman

Tobacman

2014

Journal of Biological Chemistry

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Background: Mechanism by which Wnt expression was increased by carrageenan exposure was unknown. Results: Sp1 activated Wnt9A transcription through changes in arylsulfatase B, chondroitin 4-sulfation, and galectin-3. Conclusion: Decline in arylsulfatase B leads to transcriptional effects mediated by Sp1 and galectin-3. Significance: Extracellular events can regulate transcription through changes in arylsulfatase B and chondroitin 4-sulfation.

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mentioning

confidence: 99%

Increased Expression of Colonic Wnt9A through Sp1-mediated Transcriptional Effects involving Arylsulfatase B, Chondroitin 4-Sulfate, and Galectin-3

Bhattacharyya

Feferman

Tobacman

2014

Journal of Biological Chemistry

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“…Robust expression of Wnt9b in the first arch ectoderm persists past 40hpf, surrounding the primary mouth as it initially opens at 38 -40hpf [44]. Zebrafish Wnt9b facial expression (from 24 -40 hours post fertilization) is remarkably similar to murine Wnt9b facial expression (from E9.5-11) at developmentally homologous timepoints, suggesting Wnt9b may have an integral and conserved role in vertebrate facial development across myriad taxa [38] [43]. Importantly, Wnt9b expression coincides with other signals from the pharyngeal ectodermal epithelia including the well-studied edn1 pathway (described below), so Wnt9b expression is therefore well-placed spatially and temporally to influence CNCC [45].…”

Section: Wnt Growth Factor Signalingmentioning

confidence: 99%

“…In zebrafish, we and others showed that Wnt9b is expressed maternally and during early zygotic phases [41]- [43]. Later, from about one day post fertilization (dpf) onwards, Wnt9b is expressed within the first pharyngeal arch (PA) ectodermal epithelia that overlies the arch's cranial neural crest cells (CNCCs), which have mostly finished their migration into the ventral half of the embryo by 24 hours post fertilization (hpf) [41].…”

Section: Wnt Growth Factor Signalingmentioning

confidence: 99%

“…dlx1a, dlx2a, edn1, frzb, jag1b, pitx2, sox9a, Wnt3a, and Wnt5b PCR inserts were amplified from cDNA and cloned into the pCRII TOPO vector to allow for bi-directional in vitro transcription. Wnt9a probes were generated from plasmids used in our prior publication [43]. All WISH experiments compared SB-MM (2.6 ng) control injected embryos and SB-MO (2.6ng) injected embryos.…”

Section: Wholemount In Situ Hybridization (Wish)mentioning

confidence: 99%

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Zebrafish Wnt9b Patterns the First Pharyngeal Arch into D-I-V Domains and Promotes Anterior-Medial Outgrowth

Jackson¹,

Prakash²,

Litaker³

et al. 2015

AJMB

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H. W. Jackson et al. 58pitx2a after the opening of the primary mouth and disrupted expression of Wnt5b which is consistent with disrupted chondrocyte stacking. Strong upregulation of dorsal mesodermal frzb expression in the prechordal plate of Wnt9b morphants suggests a role for Wnt9b in primary mouth induction or maintenance. Collectively these results argue that Wnt9b has a much earlier developmental requirement. This work draws attention to potential vertebrate homologies that pattern CNCC and facial outgrowth and therefore calls for a reexamination of Wnt9b's role during mammalian craniofacial development.

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“…However, the Wnt ligand responsible for initiating these downstream events remains unknown. Interestingly, a number of Wnt genes including, Wnt8b, Wnt9, Wnt5 and Wnt7 are all expressed in the zebrafish rostral forebrain (Thisse and Thisse, 2005;Danesin et al, 2009;Cox et al, 2010;Beretta et al, 2011).…”

Section: Introductionmentioning

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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Zebrafish Wnt9a,9b paralog comparisons suggest ancestral roles for Wnt9 in neural, oral–pharyngeal ectoderm and mesendoderm

Cited by 12 publications

References 29 publications

Increased Expression of Colonic Wnt9A through Sp1-mediated Transcriptional Effects involving Arylsulfatase B, Chondroitin 4-Sulfate, and Galectin-3

Increased Expression of Colonic Wnt9A through Sp1-mediated Transcriptional Effects involving Arylsulfatase B, Chondroitin 4-Sulfate, and Galectin-3

Zebrafish Wnt9b Patterns the First Pharyngeal Arch into D-I-V Domains and Promotes Anterior-Medial Outgrowth

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

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