CNBP is required for craniofacial skeleton development in zebrafish

WEINER, A; ALLENDE, M; BECKER, T. S.; CALCATERRA, NORA BEATRIZ

Rosario

Congreso; XLII Reunion Anual de la SAIB; 2006

SAIB

Striking conservation in various organisms suggests that Cellular Nucleic acid Binding Protein (CNBP) plays a fundamental biological role across different species. Recently, it was reported that CNBP is required for forebrain formation during chick and mouse embryogenesis. In this study, we have used the zebrafish model system to expand the basic understanding of CNBP activity during vertebrate head development. We show that zebrafish cnbp is expressed in a similar fashion as has been observed in early chick and mouse embryos. Using antisense morpholino oligonucleotide knock-down assays we show that CNBP depletion causes forebrain truncation while trunk development appears normal. A substantial reduction in cell proliferation and an increase in cell death were observed in the anterior regions of cnbp morphant embryos. In situ hybridization assays show that CNBP depletion does not affect CNS patterning while it does cause neural crest derivative depletion. Our data suggest an essential role for CNBP in mediating neural crest expansion by controlling proliferation and cell survival rather than via a cell fate switch during rostral head development. This possible role of CNBP may not only explain zebrafish craniofacial anomalies but also those ones reported for mice and chicken and, moreover, demonstrate that CNBP plays an essential and conserved role during vertebrate head development Striking conservation in various organisms suggests that Cellular Nucleic acid Binding Protein (CNBP) plays a fundamental biological role across different species. Recently, it was reported that CNBP is required for forebrain formation during chick and mouse embryogenesis. In this study, we have used the zebrafish model system to expand the basic understanding of CNBP activity during vertebrate head development. We show that zebrafish cnbp is expressed in a similar fashion as has been observed in early chick and mouse embryos. Using antisense morpholino oligonucleotide knock-down assays we show that CNBP depletion causes forebrain truncation while trunk development appears normal. A substantial reduction in cell proliferation and an increase in cell death were observed in the anterior regions of cnbp morphant embryos. In situ hybridization assays show that CNBP depletion does not affect CNS patterning while it does cause neural crest derivative depletion. Our data suggest an essential role for CNBP in mediating neural crest expansion by controlling proliferation and cell survival rather than via a cell fate switch during rostral head development. This possible role of CNBP may not only explain zebrafish craniofacial anomalies but also those ones reported for mice and chicken and, moreover, demonstrate that CNBP plays an essential and conserved role during vertebrate head development