Please use this identifier to cite or link to this item: https://doi.org/10.1016/j.bbamcr.2011.09.018
Title: Perturbation of zebrafish swimbladder development by enhancing Wnt signaling in Wif1 morphants
Authors: Yin, A.
Korzh, V. 
Gong, Z. 
Keywords: Hedgehog signaling
IWR-1
Swimbladder
Wif1
Wnt signaling
Zebrafish
Issue Date: Feb-2012
Citation: Yin, A., Korzh, V., Gong, Z. (2012-02). Perturbation of zebrafish swimbladder development by enhancing Wnt signaling in Wif1 morphants. Biochimica et Biophysica Acta - Molecular Cell Research 1823 (2) : 236-244. ScholarBank@NUS Repository. https://doi.org/10.1016/j.bbamcr.2011.09.018
Abstract: Wnt signaling plays critical roles in development of both tetrapod lung and fish swimbladder, which are the two evolutionary homologous organs. Our previous data reveal that down-regulation of Wnt signaling leads to defective swimbladder development. However, the effects of up-regulation of Wnt signaling on swimbladder development remain unclear. By knockdown of the Wnt protein inhibitory gene wif1, we demonstrated that up-regulation of Wnt signaling also resulted in perturbed development of the swimbladder. Specifically, the growth of epithelium and mesenchyme was greatly inhibited, the smooth muscle differentiation was abolished, and the organization of mesothelium was disturbed. Furthermore, our data reveal that it is the reduced cell proliferation, but not enhanced apoptosis, that contributes to the disturbance of swimbladder development in wif1 morphants. Blocking Wnt signaling by the Wnt antagonist IWR-1 did not affect wif1 expression in the swimbladder, but complete suppression of Hedgehog signaling in smo -/- mutants abolished wif expression, consistent with our earlier report of a negative feedback regulation of Wnt signaling in the swimbladder by the Hedgehog signaling. Our works established the importance of proper level of Wnt signaling for normal development of swimbladder in zebrafish. © 2011 Elsevier B.V.
Source Title: Biochimica et Biophysica Acta - Molecular Cell Research
URI: http://scholarbank.nus.edu.sg/handle/10635/101365
ISSN: 01674889
DOI: 10.1016/j.bbamcr.2011.09.018
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