Mode of inheritance of the low score normal condition in chickens

The abnormal muscle condition termed low score normal (LSN) was first detected in an outcross of chickens with hereditary muscular dystrophy (MD) to a commercial White Leghorn stock. At 2 to 3 mo of age, normal birds can right themselves between 15 and 20 times (exhaustion score) when placed on their back on a flat surface, whereas birds with MD cannot right themselves under similar conditions. Birds classified as LSN are intermediate to these extremes. The inheritance of the LSN abnormality has not been established. In order to determine if the LSN condition was controlled by a single gene, the LSN line was reciprocally crossed with a White Leghorn line to produce two F1 populations. Two F2 populations were produced by randomly mating individuals within each F1 population. Each F1 population was backcrossed to the White Leghorn line. When birds with an exhaustion score of 6 or less were considered LSN, ratios obtained in the F1 population were 3 normal and 134 LSN individuals for the cross of the LSN line males and White Leghorn line females, and 8 normal and 118 LSN for the reciprocal cross, suggesting that the LSN condition was influenced by a dominant gene with incomplete penetrance. The frequencies did not differ between sexes in either F1 cross, suggesting autosomal inheritance. In general, ratios of normal to LSN individuals in the two F2 populations and in the two backcross populations supported the hypothesis that the LSN trait was controlled by a dominant autosomal gene. However, there was an excess of normal females relative to that expected in the cross of the White Leghorn line males and LSN line females. Heritability (h2) of the LSN trait was estimated by regression of F2 offspring on F1 parents. The h2 estimates based on regressions were higher (range = 0.520 to 1.107) in the LSN line male x White Leghorn line female cross than in the reciprocal cross (range = 0.161 to 0.621). The h2 estimates based on regression of offspring on dams were higher for male offspring than for female offspring, suggesting the presence of sex-linked effects. It was concluded that the LSN trait was influenced primarily by an autosomal dominant gene but was also influenced by other genes, some of which were on the sex chromosome.