Glucocorticoid-induced cleft palate genes in chromosome 17: Genetic linkage and mapping analyses

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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 E βand 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 β, from E βto 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-2 aand H-2 b. 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.