Involvement of wnt signaling pathways in the metamorphosis of the bryozoan bugula neritina
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KAUST DepartmentBiological and Environmental Sciences and Engineering (BESE) Division
Computational Bioscience Research Center (CBRC)
Integrative Systems Biology Lab
KAUST Global Collaborative Research Program
Permanent link to this recordhttp://hdl.handle.net/10754/325301
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AbstractIn this study, we analyzed the metamorphosis of the marine bryozoan Bugula neritina. We observed the morphogenesis of the ancestrula. We defined three distinct pre-ancestrula stages based on the anatomy of the developing polypide and the overall morphology of pre-ancestrula. We then used an annotation based enrichment analysis tool to analyze the B. neritina transcriptome and identified over-representation of genes related to Wnt signaling pathways, suggesting its involvement in metamorphosis. Finally, we studied the temporal-spatial gene expression studies of several Wnt pathway genes. We found that one of the Wnt ligand, BnWnt10, was expressed spatially opposite to the Wnt antagonist BnsFRP within the blastemas, which is the presumptive polypide. Down-stream components of the canonical Wnt signaling pathway were exclusively expressed in the blastemas. Bn?catenin and BnFz5/8 were exclusively expressed in the blastemas throughout the metamorphosis. Based on the genes expression patterns, we propose that BnWnt10 and BnsFRP may relate to the patterning of the polypide, in which the two genes served as positional signals and contributed to the polarization of the blastemas. Another Wnt ligand, BnWnt6, was expressed in the apical part of the pre-ancestrula epidermis. Overall, our findings suggest that the Wnt signaling pathway may be important to the pattern formation of polypide and the development of epidermis. © 2012 Wong et al.
CitationWong YH, Wang H, Ravasi T, Qian P-Y (2012) Involvement of Wnt Signaling Pathways in the Metamorphosis of the Bryozoan Bugula neritina. PLoS ONE 7: e33323. doi:10.1371/journal.pone.0033323.
PublisherPublic Library of Science (PLoS)
PubMed Central IDPMC3308966
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