Lysyl oxidase-like 3b is Critical for Cartilage Maturation During Zebrafish Craniofacial Development
- van Boxtel, A.L., Gansner, J.M., Hakvoort, H.W., Snell, H., Legler, J., and Gitlin, J.D.
- Matrix biology : journal of the International Society for Matrix Biology 30(3): 178-87 (Journal)
- Registered Authors
- Gitlin, Jonathan D., Legler, Juliette, Snell, Heather
- zebrafish, lysyl oxidase, cartilage, craniofacial development
- MeSH Terms
- Amino Acid Oxidoreductases/genetics
- Amino Acid Oxidoreductases/metabolism*
- Body Patterning/genetics
- Cell Death
- Cell Differentiation/genetics
- Cell Proliferation
- Cell Shape/genetics
- Cloning, Molecular
- Extracellular Matrix/genetics
- Extracellular Matrix/ultrastructure
- Gene Silencing
- Neural Crest/cytology
- Neural Crest/metabolism
- Stem Cells/cytology
- Zebrafish Proteins/genetics
- Zebrafish Proteins/metabolism*
- 21244857 Full text @ Matrix Biol.
van Boxtel, A.L., Gansner, J.M., Hakvoort, H.W., Snell, H., Legler, J., and Gitlin, J.D. (2011) Lysyl oxidase-like 3b is Critical for Cartilage Maturation During Zebrafish Craniofacial Development. Matrix biology : journal of the International Society for Matrix Biology. 30(3):178-87.
Vertebrate craniofacial development requires coordinated morphogenetic interactions between the extracellular matrix (ECM) and the differentiating chondrocytes essential for cartilage formation. Recent studies reveal a critical role for specific lysyl oxidases in ECM integrity required for embryonic development. We now demonstrate that loxl3b is abundantly expressed within the head mesenchyme of the zebrafish and is critically important for maturation of neural crest derived cartilage elements. Histological and ultrastructural analysis of cartilage elements in loxl3b morphant embryos reveals abnormal maturation of cartilage and altered chondrocyte morphology. Spatiotemporal analysis of craniofacial markers in loxl3b morphant embryos shows that cranial neural crest cells migrate normally into the developing pharyngeal arches but that differentiation and condensation markers are aberrantly expressed. We further show that the loxl3b morphant phenotype is not due to P53 mediated cell death but likely to be due to reduced chondrogenic progenitor cell proliferation within the pharyngeal arches. Taken together, these data demonstrate a novel role for loxl3b in the maturation of craniofacial cartilage and can provide new insight into the specific genetic factors important in the pathogenesis of craniofacial birth defects.
Genes / Markers
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Engineered Foreign Genes