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

Hofmeister, Wolfgang and Key, Brian (2013) Frizzled-3a and Wnt-8b genetically interact during forebrain commissural formation in embryonic zebrafish. Brain Research, 1506 25-34. doi:10.1016/j.brainres.2013.02.028

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Author Hofmeister, Wolfgang
Key, Brian
Title Frizzled-3a and Wnt-8b genetically interact during forebrain commissural formation in embryonic zebrafish
Formatted title
Frizzled-3a and Wnt-8b genetically interact during forebrain commissural formation in embryonic zebrafish
Journal name Brain Research   Check publisher's open access policy
ISSN 0006-8993
1872-6240
Publication date 2013-04-19
Year available 2013
Sub-type Article (original research)
DOI 10.1016/j.brainres.2013.02.028
Open Access Status File (Author Post-print)
Volume 1506
Start page 25
End page 34
Total pages 10
Place of publication Amsterdam, Netherlands
Publisher Elsevier
Collection year 2014
Language eng
Formatted abstract
The 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.
Keyword Wnt8b
Fzd3a
Axon guidance
Commissure
Zebrafish
Slit2
Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
Collections: Official 2014 Collection
School of Biomedical Sciences Publications
 
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