Noggin is required for first pharyngeal arch differentiation in the frog Xenopus tropicalis
| Autor: | John J. Young, Gloria Wu, Shu-wei Hsu, Richard M. Harland, Daniel Wong, Rachel A. S. Kjolby |
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| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
Follistatin Embryo Nonmammalian Morpholino Xenopus Mandible Xenopus Proteins Medical and Health Sciences Morpholinos Gene Knockout Techniques 0302 clinical medicine Pediatric Nonmammalian biology Homozygote Cell Differentiation Biological Sciences Cell biology medicine.anatomical_structure Embryo Larva embryonic structures Bone Morphogenetic Proteins Intercellular Signaling Peptides and Proteins Neural development medicine.medical_specialty Mesoderm animal structures 1.1 Normal biological development and functioning Bone morphogenetic protein Article 03 medical and health sciences Underpinning research Internal medicine medicine Genetics Animals Noggin Dental/Oral and Craniofacial Disease Molecular Biology Alleles Glycoproteins Body Patterning Skull Neural tube Cell Biology biology.organism_classification 030104 developmental biology Endocrinology Cartilage Branchial Region biology.protein Carrier Proteins 030217 neurology & neurosurgery Developmental Biology |
| Zdroj: | Developmental biology, vol 426, iss 2 |
| Popis: | The dorsal ventral axis of vertebrates requires high BMP activity for ventral development and inhibition of BMP activity for dorsal development. Presumptive dorsal regions of the embryo are protected from the ventralizing activity of BMPs by the secretion of BMP antagonists from the mesoderm. Noggin, one such antagonist, binds BMP ligands and prevents them from binding their receptors, however, a unique role for Noggin in amphibian development has remained unclear. Previously, we used zinc-finger nucleases to mutagenize the noggin locus in Xenopus tropicalis. Here, we report on the phenotype of noggin mutant frogs as a result of breeding null mutations to homozygosity. Early homozygous noggin mutant embryos are indistinguishable from wildtype siblings, with normal neural induction and neural tube closure. However, in late tadpole stages mutants present severe ventral craniofacial defects, notably a fusion of Meckel's cartilage to the palatoquadrate cartilage. Consistent with a noggin loss-of-function, mutants show expansions of BMP target gene expression and the mutant phenotype can be rescued with transient BMP inhibition. These results demonstrate that in amphibians, Noggin is dispensable for early embryonic patterning but is critical for cranial skeletogenesis. |
| Databáze: | OpenAIRE |
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