Integrated GWAS and transcriptome analysis provide molecular insights into the resistance to Streptococcus iniae in yellowfin seabream, Acanthopagrus latus (Hottuyn, 1782)

In recent years, the aquaculture industry of yellowfin seabream ( Acanthopagrus latus ) has been severely threatened by infections caused by Streptococcus iniae . Selective breeding for disease resistance has emerged as an effective strategy to address this challenge. To further elucidate the genetic basis of this trait, we conducted S. iniae infections on 2000 individual yellowfin seabreams and performed whole-genome resequencing on the first 80 deceased individuals exhibiting infection symptoms and the last 80 surviving individuals. The estimated heritability of disease resistance was 0.233 ± 0.03. Using a genome-wide association study (GWAS), we analyzed disease resistance as a binary phenotype. Our analysis identified nine single nucleotide polymorphisms (SNPs) that were significantly associated with S. iniae resistance. Notably, one SNP is located in the exonic region of PTP-βL with the missense mutation, one in the intronic region of Il12rb1 , and one downstream of NLRP3l . Previous studies have shown that these genes are associated with immune responses. Additionally, we performed transcriptome analysis of the livers samples of yellowfin seabreams 72 h post-infection, revealing 1614 differentially expressed genes (1130 significantly upregulated and 484 significantly downregulated) compared to the PBS injection control group. KEGG and GO enrichment analyses of the DEGs identified numerous immune-related terms. Finally, we found that PTP-βL was present in both the GWAS candidate genes and the DEGs. Our findings provide potential genetic variations and gene targets for molecular marker-assisted selection to improve disease resistance in yellowfin seabream, offering valuable insights for advancing disease resistance mechanisms in aquaculture fish species. • GWAS and RNAseq were jointly employed to identify candidate genes. • Nine SNPs were found to be significantly associated with SI resistance traits. • A significantly associated missense mutation in PTP-βL was observed, accompanied by differential expression. • The heritability estimate for the SI resistance trait was 0.233 ± 0.03.