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Cattle exhibit a range of carcass defects, including blood splash (BLS), intramuscular edema (INE), muscle steatosis (MUS), bruising (BR), trim loss (TRL) and others (OTH). These defects lower the carcass value and can result in significant economic loss to producers. We estimated the incidence, relationship with inbreeding coefficients and genetic parameters of carcass defects in Japanese Black cattle using 561 619 carcass records from Kagoshima, Japan during April 1988 through March 2011. The defect incidence ranged from 0.22% for TRL to 5.73% for BR. The incidence of MUS and BR increased from 1.21% to 6.57% and from 1.06% to 9.31%, respectively. The incidence of INE peaked at 7.44% in 1999 and decreased thereafter. We observed a positive linear relationship between the defect incidence and the inbreeding coefficients in MUS, BR and TRL (P < 0.01). The heritabilities estimated by univariate animal model with Gibbs sampling for BLS, INE, MUS, BR and TRL were 0.24, 0.06, 0.18, 0.05 and 0.02, respectively. The contribution of farm variance to phenotypic variance was negligible (0.01 to 0.04). Significant genetic correlations of TRL were estimated with MUS (0.63) and BR (0.63). Our results suggest that genetic factors contribute to the incidence of BLS and MUS.

Polymorphisms in the prion protein gene (PRNP) are known to be associated with transmissible spongiform encephalopathies in human, sheep and goats. There is tentative association between PRNP promoter polymorphism and bovine spongiform encephalopathy (BSE) susceptibility in cattle. In this study, we genotyped for six bovine PRNP polymorphic sites including a 23-bp indel in the promoter, a 12-bp indel in the intron 1, two nonsynonymous single nucleotide polymorphisms (SNPs), octapeptide repeats in the coding region and a 14-bp indel in the 3'-untranslated region in 178 animals representing Japanese Brown, Kuchinoshima feral, Mishima, Japanese Shorthorn and Holstein. In 64 Japanese Brown cattle, three indel sites were polymorphic. All of the six sites were monomorphic in Kuchinoshima. The 23-bp and 12-bp indel sites were polymorphic in Mishima cattle. The 23-bp and 14-bp indel sites were polymorphic in Japanese Shorthorn cattle. Both SNP sites were monomorphic in all cattle examined in this study. At the 23-bp indel site, the genotype frequencies of Japanese Brown and Holstein breeds were similar to that of BSE affected cattle. We estimated 12 different haplotypes from these genotypic data. A '23-12-K6S14+' haplotype was the major haplotype in all populations, whose frequencies ranged from 0.50 to 1.00.

The gene constitution of polymorphisms of the four calpain genes (µ-calpain, m-calpain, p94, and µ/m-calpain) were analyzed in South-East Asian native chickens, White Leghorn and Broiler commercial chickens, and Red and Green jungle fowl. Polymorphisms were detected at all loci in chickens and Red jungle fowl, but only for CAPN1 (µ-calpain gene) in Green jungle fowl. CAPN2 and CAPN1.5 are linked on chicken chromosome 3, and the genotype for these loci were treated as haplotype. Some combinations of calpain loci were tested using principal component analysis, and the best combination (CAPN1, CAPN3, and CAPN1.5) was determined. The proportion of polymorphic loci (Ppoly) and heterozygosity ( ) were 1.00 and 0.316‐0.465 in domestic chickens and red jungle fowl, and 0.33 and 0.137 in Green jungle fowl, respectively. GST values suggested that the degree of subdivision among native chickens was relatively low except for Thailand, which was highest. Pair-wise FST testing, dendrogram and principal component analysis from the results of calpain loci showed that the four South-East Asian native and commercial chicken populations were close genetically.

Calpains are intracellular Ca2+-dependent proteases and enzymes that contribute to growth and meat quality. In the present study, we identified polymorphisms in four calpain genes (CAPN1, CAPN2, CAPN3, and CAPN1.5) expressed ubiquitously in chicken using polymerase chain reaction-restriction fragment length polymorphism, and mapped them using two backcross families (East Lansing (EL) and Kobe University (KU)). CAPN2 and CAPN1.5 mapped to two locations on chromosome 3 about 30 cM apart, while CAPN3 mapped to chromosome 5. CAPN1 was linked to a previously unlinked microsatellite marker LEI0140 to form a new linkage group called E66. CAPN2 and CAPN3 extend the amount of conserved synteny between chicken chromosome 3 and human chromosome 1, and between chicken chromosome 5 and human chromosome 15, respectively. Although CAPN2, CAPN3, and CAPN1.5 were found in the University of California Santa Cruz chicken genome browser gateway, CAPN1 and LEI0140 were not in specific genomic positions.

Three electrophoretic variations (AA, BB and AB) of ovalbumin controlled by codominant alleles OvA and OvB have been observed in various chicken populations. We compared nucleotide sequences of the open reading frame between two alleles of ovalbumin gene. The difference between the two alleles was found as a non-synonymous substitution of asparagine to aspartic acid as a result of AAT to GAT point mutation at position 8032–8034 in exon 8. We developed polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) protocol in combination with Mbo I restriction endnuclease mapping for the detection of this substitution. By the PCR-RFLP the allelic frequency of the OvB was estimated to be within the range of 0.000–0.150 in 11 Asian indigenous chicken populations and 0.000 in four improved breeds used in the present study. Gene frequency, estimated by PCR-RFLP in the present study, paralleled that obtained by protein polymorphisms of egg white. Thus, this study provides, for the first time, information of the occurrence of ovalbumin allele OvA and OvB in Asian indigenous chicken populations.