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Analysis of Neural Crest Migration and Differentiation by Cross-species Transplantation
Published on: February 7, 2012
Placode-derived orphan chemokine CXCL14 is critical for proper chick trigeminal ganglion formation
Hugo A Urrutia1, Junpeng Gao1, Marianne E Bronner1
1Division of Biology and Biological Engineering, California Institute of Technology, Pasadena, CA, 91125, USA.
Insights
The study reveals that chemokine CXCL14 is crucial for trigeminal ganglion development in chick embryos. Knocking out CXCL14 disrupts ganglion formation and axonal projections, suggesting a novel CXCR4/CXCL14 interaction.
Area of Science:
- Developmental Biology
- Neuroscience
- Molecular Biology
Background:
- The trigeminal ganglion originates from neural crest and ectodermal placode cells.
- Understanding the molecular mechanisms guiding cranial sensory ganglion formation is essential.
Purpose of the Study:
- To investigate the role of chemokines in trigeminal ganglion development.
- To identify novel ligand-receptor interactions involved in this process.
Main Methods:
- CRISPR-Cas9 mediated knockout of Cxcl14 in developing chick embryos.
- Analysis of trigeminal ganglion formation, lobe development, and axonal projections.
- Expression analysis of Cxcl14 and Cxcr4.
Main Results:
- Cxcl14 is expressed in placode-derived cells during trigeminal ganglion condensation.
- Cxcl12, the canonical Cxcr4 ligand, is expressed in distant regions.
- Cxcl14 knockout leads to disrupted trigeminal ganglion formation, including loss of the maxillomandibular lobe and reduced ophthalmic lobe.
- Axonal projection defects were observed in Cxcl14 knockout embryos.
Conclusions:
- Cxcl14 plays a critical in vivo role in trigeminal ganglion development.
- A novel ligand-receptor interaction between CXCR4 and CXCL14, not CXCL12, is implicated in trigeminal ganglion formation.
Abstract:
The trigeminal ganglion, the largest of cranial sensory ganglia, has a dual origin from neural crest and ectodermal placode cells, which interact extensively during ganglion formation. In the developing chick embryo, we find that the orphan chemokine Cxcl14 is expressed in placode-derived cells at a time corresponding to when placode and neural crest cells, expressing the chemokine receptor Cxcr4, begin to condense into the trigeminal ganglion. In contrast, Cxcl12, the proposed canonical receptor for Cxcr4, is expressed in the frontonasal process and branchial arches, regions distant from the forming ganglion primordium. Importantly, CRISPR-Cas9 mediated knockout of Cxcl14 disrupted trigeminal ganglion formation, resulting in loss of the maxillomandibular lobe and reduction in the ophthalmic lobe as well as defective axonal projections. Taken together, these data reveal a new in vivo role for Cxcl14 during development and suggest a ligand-receptor interaction between CXCR4 and CXCL14, rather than CXCL12, during trigeminal ganglion development.
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