Phenotypic measurements of chicken egg character and production traits are restricted to mature females only. Marker assisted selection of immature chickens using quantitative trait loci (QTL) has the potential to accelerate the genetic improvement of these traits in the chicken population. The QTL for 12 traits (i.e. body weight (BW), six for egg character, three for egg shell colour and two for egg production) of chickens were identified. An F2 population comprising 265 female chickens obtained by crossing White Leghorn and Rhode Island Red breeds and genotyped for 123 microsatellite markers was used for detecting QTL. Ninety-six markers were mapped on 25 autosomal linkage groups, and 13 markers were mapped on one Z chromosomal linkage group. Eight previous unmapped markers were assigned to their respective chromosomes in this study. Significant QTL were detected for BW on chromosomes 4 and 27, egg weight on chromosome 4, the short length of egg on chromosome 4, and redness of egg shell colour (using the L*a*b* colour system) on chromosome 11. A significant QTL on the Z chromosome was linked with age at first egg. Significant QTL could account for 6-19% of the phenotypic variance in the F2 population.

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In the outbreak of abortions, premature births, stillbirths and congenital arthrogryposis-hydranencephaly (AH) syndrome in Japan during the summer through winter of 1972-73 and 1973-74, precolostral sera from calves with congenital AH syndrome and normal calves were tested for neutralizing antibodies against some arboviruses, i.e. Akabane, Aino, Getah and Japanese encephalitis (JE) viruses. The incidence of antibody for Akabane virus was very high in calves with AH syndrome (49/59 or 83 per cent) as compared with normal calves (3/11 or 27 per cent), indicating an intimate correlation between the AH syndrome and precolostral anti-Akabane antibody. Three stillborn fetuses also had anti-Akabane antibody. On the other hand, no precolostral serum antibody for the other viruses was detected in any of the calves tested. The mothers of these calves, normal and with AH syndrome, had anti-Akabane antibody in high percentages (44/52 or 85 per cent and 7/8 or 88 per cent), whereas a few of the mothers had antibodies for the other viruses. Serological surveys indicate a wide dissemination of Akabane virus in epizootic areas during the summer months of 1972 and 1973. Thus, 8 groups of cattle in epizootic areas showed high rates of seroconversion for Akabane virus during the 1972 or 1973 summer. Very high incidences of Akabane antibody were shown among cattle in epizootic areas but extremely low incidences in near-by non-epizootic areas. The geographic distribution of anti-Akabane antibody among cattle throughout the country in the 1973 spring generally agrees with the pattern of case distribution in the 1972--73 outbreak. All these findings strongly suggest that Akabane virus is the etiological agent of the outbreaks. Further studies are needed, particularly isolation of the virus, demonstration of infection with the virus in lesions by immunofluroescence and production of intrauterine infection by experimental infection of pregnant cows.

We performed a quantitative trait locus (QTL) analysis to map QTLs controlling shank length, body weight, and carcass weight in a resource family of 245 F₂ birds developed from a cross of the large-sized, native, Japanese cockfighting breed, Oh-Shamo (Japanese Large Game), and the White Leghorn breed of chickens. Interval mapping revealed three significant QTLs for shank length on chromosomes 1, 4 and 24 at the experiment-wise 5% level, and a suggestive shank length QTL on chromosome 27 at the experiment-wise 10% level. For body weight two QTLs, one significant and the other suggestive, were identified on chromosomes 4 and 24, respectively. As expected, QTLs for carcass weight, which was highly correlated with body weight (r = 0.95), were detected at the same chromosomal locations as the detected body weight QTLs. Interestingly, the chromosomal locations containing these body weight and carcass weight QTLs coincided with those of two of the four shank length QTLs detected. No QTL with an epistatic interaction effect was discovered for any trait. The total contribution of all detected QTLs to genetic variance was 98.4%, 27.0% and 25.9% for shank length, body weight and carcass weight, respectively, indicating that most shank length QTLs have been identified but many body weight and carcass weight QTLs have been overlooked by the present analysis because of a low coverage rate of the 88 microsatellite markers used here (approximately 46% of the whole genome).