ABNORMAL FACIAL DEVELOPMENT IN THE MOUSE MUTANT 1ST ARCH

  • 1 January 1983
    • journal article
    • research article
    • Vol. 3  (4) , 317-337
Abstract
The 1st arch mutation in mice, far, causes specific severe craniofacial defects, different from those caused by other craniofacial mutations. To define the facial defects in far homozygotes, to identify heterozygote expression, if any, and to investigate the embryogenisis of the defect, a genetic study and a developmental stydy were done. The genetic study showed that only far homozygotes, observed on day 18 of gestation, have cleft palate, pointed snout, and deficiency and disorganized pattern of maxillary vibrissae. Approximately 75% have open eye(s). In addition, only far homozygotes lack infraorbital vibrissa(e) (76%) or have facial skin tags (62%). The missing infraorbital vibrissa(e) and disturbed maxillary vibrissa pattern could be used to identify far/far embryos for developmental study. The developmental study showed that all of the defects observed in far homozygotes at birth can be accounted for by abnormalities present on day 12 of gestation. Palatal shelves and vibrissal ridges are deficient and irregular. Maxillary branch of the trigeminal nerve is abnormal and associated with a streaming and swirling pattern of mesenchymal cells between vibrissae and palate. No aberrations in cell density are apparent on day 12. The primary defect in the far mutation is not known but all of the defects derive specifically from the maxillary facial process, 1 portion of the 1st branchial arch.

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