Abstract
A line of new plumage color mutation of the Japanese quail has been established in our laboratory. This mutation is inherited by a simple autosomal gene (rs) and is recessive to the wild type. Female homozygotes (rs/rs) showed dysfunction in albumen secretion, egg shell formation, and consequently egg laying, whereas male homozygotes showed no reproductive failure.
Analysis of the oviducal secreta of rs/rs female by crossed-immunoelectrophoresius sing a polyspecific anti-albumen serum showed that the amount of albumen secreted into the oviduct magnum of the mutant is negligibly small.
The tissue samples of the oviduct magnum taken from the ovariectomized (OVX) mutant quail treated with estradiol benzoate (EB, 0.1mg/day for 5 days) were homogenized and their ovalbumin content was estimated by rocket immunoelectrophoresis. In these samples the amount of ovalbumin was comparable to that found in the oviduct of the widetype quail, which indicates that the oviduct magnum of the mutant can respond to EB normally as far as ovalbumin synthesis is concerned.
Avidin, a progesterone (P) dependent protein, was detected at the oviduct magnum of the adult mutant as well as laying wild-type females by histochemical staining using biotinyl-horseradish peroxidase method. Although the synthesis of avidin was not induced by EB treatment alone in oviduct magnum of the OVX mutant nor in that of the OVX wild-type quail, the birds primed by EB then injected with P (0.1mg) initiated the synthesis of avidin without regard to their phenotypes. These results indicate that the failure in albumen deposition peculiar to rs/rs quail is attributed to their inability for releasing but not for the synthesis of the albumen.
