Glucocorticoid-induced cleft palate genes in chromosome 17: Genetic linkage and mapping analyses |
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Authors: | Joseph J. Bonner Marvin L. Tyan |
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Affiliation: | (1) The Dental Research Institute, University of California, 90024 Los Angeles, California;(2) Medical and Research Services, Veterans Administration, West Los Angeles Medical Center, Los Angeles, California;(3) Department of Medicine, UCLA School of Medicine, Los Angeles, California |
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Abstract: | Genes that influence susceptibility to dexamethasone-induced cleft palate and tentatively designated Dcp are linked to the major histocompatibility complex H-2 in chromosome 17 of the mouse. Experiments presented refine the map of genes. The results show two or three Dcp loci. The two-locus model maps Dcp genes to the class II gene Eand to the chromosomal region between the S and D genes. The three-locus model maps the Dcp genes to the chromosomal regions from the centromere to E, from Eto S, and from D to Pgk-2. Experiments were done by comparing the dexamethasone-induced cleft palate dose response of congenic strains with H-2 haplotypes that are recombinants of H-2aand H-2b. The analysis of genetic linkage between H-2 and Dcp was expanded to include reciprocal backcrosses. A maternal factor was found to influence the frequency of dexamethasone-induced cleft palate in the backcross fetuses. The factor's origin is associated with the H-2 haplotype of the outcross mother, so the effect is actually a grandmother effect that probably is transmitted horizontally. Finally, the sexes were distributed unevenly between the fetuses with cleft palate in two of the congenic strains. This suggests interaction between the H-2-linked Dcp genes and a Dcp sex-associated gene that modulates susceptibility to dexamethasone-induced cleft palate. |
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