| First Author | Bonner JJ | Year | 1984 |
| Journal | Immunogenetics | Volume | 20 |
| Issue | 2 | Pages | 169-83 |
| PubMed ID | 6469287 | Mgi Jnum | J:7547 |
| Mgi Id | MGI:56017 | Doi | 10.1007/BF00364488 |
| Citation | Bonner JJ, et al. (1984) Glucocorticoid-induced cleft palate genes in chromosome 17: genetic linkage and mapping analyses. Immunogenetics 20(2):169-83 |
| abstractText | Genes that influence susceptibility to dexamethasone-induced cleft palate and tentatively designated Dep 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 Dep loci. The two-locus model maps Dep genes to the class II gene E beta and to the chromosomal region between the S and D genes. The three-locus model maps the Dep genes to the chromosomal regions from the centromere to E beta, from E beta to 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-2a and H-2b. The analysis of genetic linkage between H-2 and Dep 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 Dep genes and a Dep sex-associated gene that modulates susceptibility to dexamethasone-induced cleft palate. |
