Genetic Transmission of Congenital Membranous Ventricular Septal Defects in Selectively Inbred Substrains of Rats
Two inbred substrains of Long-Evans rats have been maintained under identical laboratory conditions. In one substrain (Olson-Goss) 25% of the neonates have spontaneously occurring membranous ventricular septal defects; in the other (California) only 4% are affected. Since a genetic etiology was indicated, two series of reciprocal crosses were made to evaluate the possibilities that the defects might result from an abnormal fetal genotype, a genetically abnormal intrauterine environment, or both. In both series parents of a highly defective litter ("high-incidence" pairs) were reciprocally mated to parents of a completely normal litter ("low-incidence" pairs). In Series I, all parental pairs were Olson-Goss animals; in Series II, the low-incidence pairs were California animals. Substitution of a low- for a high-incidence male consistently and appreciably decreased the incidence of defects in the progeny of high-incidence females. Conversely, low-incidence females produced a relatively large number of defective pups when mated to high-incidence males. These data suggest that the primary factor responsible for septal malformation is the fetal genotype rather than the intrauterine environment. Patroclinous reciprocal cross differentials, particularly marked in the substrain crosses, suggest, however, that secondary factors may also be implicated.
- intrauterine influence
- reciprocal crosses
- abnormal fetal genotype
- paternal dominance in transmission
- Long-Evans rats
- © 1967 American Heart Association, Inc.