Domesticated sheep have been exposed to artificial selection for the production of fiber, meat, and milk as well as to natural selection. Such selections are likely to have imposed distinctive selection signatures on the sheep genome. Therefore, detecting selection signatures across the genome may help elucidate mechanisms of selection and pinpoint candidate genes of interest for further investigation. Here, detection of selection signatures was conducted in three sheep breeds, Sunite (n=66), German Mutton (n=159), and Dorper (n=93), using the Illumina OvineSNP50 Genotyping BeadChip array. Each animal provided genotype information for 43 273 autosomal single nucleotide polymorphisms (SNPs). We adopted two complementary haplotype-based statistics of relative extended haplotype homozygosity (REHH) and the cross-population extended haplotype homozygosity (XP-EHH) tests. In total, 707, 755, and 438 genomic regions subjected to positive selection were identified in Sunite, German Mutton, and Dorper sheep, respectively, and 42 of these regions were detected using both REHH and XP-EHH analyses. These genomic regions harbored many important genes, which were enriched in gene ontology terms involved in muscle development, growth, and fat metabolism. Fourteen of these genomic regions overlapped with those identified in our previous genome-wide association studies, further indicating that these genes under positive selection may underlie growth developmental traits. These findings contribute to the identification of candidate genes of interest and aid in understanding the evolutionary and biological mechanisms for controlling complex traits in Chinese and western sheep.

Pasteurella multocida, a Gram-negative nonmotile coccobacillus, is the causative agent of fowl cholera, bovine hemorrhagic septicemia, enzoonotic pneumonia and swine atropic rhinitis. Two filamentous hemagglutinin genes, fhaB1 and fhaB2, are the potential virulence factors. In this study, an inactivation fhaB1 mutant of P. multocida in avian strain C48-102 was constructed by a kanamycin-resistance cassette. The virulence of the fhaB1 mutant and the wild type strain was assessed in chickens by intranasal and intramuscular challenge. The inactivation of fhaB1 resulted in a high degree of attenuation when the chickens were challenged intranasally and a lesser degree when challenged intramuscularly. The fhaB1 mutant and the wild type strain were investigated their sensitivity to the antibody-dependent classical complement-mediated killing pathway in 90% convalescent chicken serum. The fhaB1 mutant was serum sensitive as the viability has reduced between untreated serum and heat inactivated chicken serum (P<0.007). These results confirmed that FhaB1 played the critical roles in the bacterial pathogenesis and further studies were needed to investigate the mechanism which caused reduced virulence of the fhaB1 mutant.