| As a common genetic disease, pig scrotal hernia has brought great losses to the modern pig industry. It is necessary for us to decipher the molecular mechanism of scrotal hernia and develop the corresponding molecular techniques for disease-resistance breeding, which contributing to reduce the incidence of pig scrotal hernia as well as cultivating disease-resistant new line pigs. The progress on molecular mechanism for pigs scrotal hernia, will give us a profound insight to study human diseases as well.In this study, a genome-wide association study(GWAS)was conducted in established previoysly a White Duroc×Erhualian resource family, Which including23F2scortal hernia pigs. A total of chromosomed-wide81significant SNPs on SSC2,8,17, were identified to be associated with pig scrotal hernia. There are79susceptibility loci intensively distributed in the region of47.17-51.37Mb on SSC17, in which, the most promising locus was MIGA0022174with the lop(1/p) value of5.44. The other two relevant SNPs were located on SSC2and SSC8, respectively. Of all associated loci, only one on SSC2was consistant with the results provided by other groups previously.6positional candidate genes including KIF3ã€TMEM156on SSC8, and EYA2, MYBC2, TNNC2, TOMM34, which all locatied in prominent region on SSC17, were explored the relationship with pig scrotal hernia in50nucleus F2/F3families in this resource families.6significant SNPs were detected by TDT analysis and further performed replication testing in outbreed trio families with102affected individuals, together with8susceptibility SNPs identified by GWAS on SSC17. The results showed only two loci c.74G>G in TNNC2and ACGA0095542in FISC36, were verified to be weakly associated with pig scrotal hernia. The further study for these two genes should be conducted to detail their functions on the etiopathogenesis of pig scrotal hernia. |