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Related Experiment Videos

Is Far a Hox mutation?

D M Juriloff1, M J Harris, J E Miller

  • 1Department of Medical Genetics, University of British Columbia, Vancouver, Canada.

Journal of Craniofacial Genetics and Developmental Biology
|July 1, 1992
PubMed
Summary
This summary is machine-generated.

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The mouse First arch mutation (Far) causes craniofacial defects, specifically abnormal maxillary nerve bifurcation. Ectopic cartilage in Far mutants may explain this nerve defect, suggesting an atavistic posteriorization.

Area of Science:

  • Developmental Biology
  • Craniofacial Development
  • Genetics

Background:

  • The mouse First arch mutation (Far) results in severe craniofacial defects, primarily affecting the anterior first branchial arch.
  • The Far mutation is linked to the Hox-4 gene cluster on chromosome 2.
  • The precise developmental origin of the maxillary nerve defect in Far mutants is not fully understood.

Purpose of the Study:

  • To investigate the developmental basis of the abnormal maxillary nerve bifurcation observed in Far mutants.
  • To explore the role of retinoic acid and neural crest segmentation in the Far-associated nerve defect.
  • To determine the significance of ectopic cartilage in the palate of Far mutants.

Main Methods:

  • Nerve-stained whole-mount preparations of day 12 Far mutant embryos.

Related Experiment Videos

  • Maternal administration of retinoic acid to assess its teratogenic effects on maxillary nerve development.
  • Examination of rhombomere segmentation in Far mutant embryos.
  • Histological analysis of palatal tissues in Far mutant fetuses.
  • Main Results:

    • Far mutants exhibit a distinct "missing wedge" in the maxillary nerve's fan shape, with defects potentially equally severe in Far/Far and +/Far genotypes.
    • Maternal retinoic acid treatment did not induce Far-like maxillary nerve defects in wild-type or heterozygous embryos.
    • No defects in rhombomere segmentation or morphology were detected in Far mutant embryos.
    • Ectopic cartilage, resembling Meckel's cartilage, was found lateral to the palate in five out of six Far/Far fetuses, situated between the bifurcated maxillary nerve trunks.

    Conclusions:

    • The abnormal maxillary nerve bifurcation in Far mutants may be caused by an ectopic precartilaginous blastema.
    • The presence of ectopic cartilage suggests a potential atavistic posteriorization of the anterior first branchial arch in Far mutants.
    • The Far mutation provides a model for studying craniofacial development and the origins of nerve malformations.