Influence of sex‐linked genes on embryonic sensitivity to cortisone in three strains of mice

Abstract

It was postulated that sex‐linked genes affecting embryonic sensitivity to cortisone‐induced cleft palate and cortisone‐induced resorption might differ between inbred mouse strains showing pronounced reciprocal effects. The three strains tested were the A/J (A), C57BL/6J (B), and C3H/HeJ (C), whose sensitivities to cortisone‐induced cleft palate had been shown to be: A > C > B. The sensitivity of reciprocal A × B and B × C hybrid embryos was matroclinous; of reciprocal A × C embryos, patroclinous. Backcrosses of reciprocal F1 hybrid males to inbred females were used to test the hypothesis of sex‐linkage with respect to the incidence of cortisone‐induced cleft palate, cortisone‐induced resorption, and the overall level of cortisone‐induced fetal damage. The results were consistent with the hypothesis that sex‐linked genes affecting embryonic sensitivity to cortisone‐induced cleft palate, but not to cortisone‐induced resorption, differ in the three strains.

Effects of the Ay Gene on the Sensitive Periods of Hydrocortisone‐Induced Cleft Palate and Palatal Slit in Mice

“…Susceptibility to the teratogenic actions of glucocorticoids is modified by substituting a single gene (Bonner and Slavkin, 1975;Francis, 1973;Gasser et al, 1981;Liu and Erickson, 1986;Marazita et al, 1988;Vekemans et al, 1981) or genetic constitution as indicated by the strain-difference studies (Fraser and Fainstat, 195 1;Kalter, 1954). In the present experiment, sensitive periods of hydrocortisone-induced palatal defects were compared between AY/a and a/a fetuses by using the single-dose administration method.…”

“…Prenatal administration of cortisone, a glucocorticoid, is known to result in palatal defects such as cleft palate and palatal slit in mouse fetuses. The teratogenic action of this hormone differs with mouse strains (Fraser and Fainstat, 1951; Kalter, 1954) and can be modified by several genes, e.g., histocompatibility- 3-linked genes on chromosome 2 (Gasser et al, 1981;Liu and Erickson, 1986), phosphoglucomutase-1 on chromosome 5 (Vekemans et al, 1981), short ear on chromosome 9 (Marazita et al, 1988), histocompatibility-2 (H-2) complex on chromosome 17 (Bonner and Slavkin, 1975), and some genes on the sex chromosome (Francis, 1973).…”

Correlation of susceptibility to 6-aminonicotinamide and hydrocortisone-induced cleft palate

“…It has been established that genetically different mouse strains exhibit different degrees of susceptibility to steroid-induced cleft palate (Fraser and Fainstat, 1951;Fraser et al, 1957;Kalter, 1954;Francis, 1973). In some strains, the H-2 or major histocompatibility complex (MHC) region has been implicated by the use of congenic strains (Bonner and Slavkin, 1975;Tyan and Miller, 1978;Erickson et al, 1979;Gasser et al, 1981Gasser et al, , 1991Gasser, 1994;Goldman et al, 1982;Melnick et al, 1981;Tyan and Tyan, 1993), and by analyses of backcrosses (Biddle and Fraser, 1977;Tyan, 1982, 1983;Tyan and Tyan, 1993).…”

“…In some strains, the H-2 or major histocompatibility complex (MHC) region has been implicated by the use of congenic strains (Bonner and Slavkin, 1975;Tyan and Miller, 1978;Erickson et al, 1979;Gasser et al, 1981Gasser et al, , 1991Gasser, 1994;Goldman et al, 1982;Melnick et al, 1981;Tyan and Tyan, 1993), and by analyses of backcrosses (Biddle and Fraser, 1977;Tyan, 1982, 1983;Tyan and Tyan, 1993). Genetic analyses have shown, however, that the differences between inbred strains of mice with respect to their incidences of steroid-induced cleft palate cannot be explained by only one or two genetic factors (Kalter, 1954;Francis, 1973;Biddle and Fraser, 1977;Liu and Erickson, 1986b).…”