Genetic diversity, population structure, linkage disequilibrium and GWAS for resistance to WSSV in Pacific white shrimp (Litopenaeus vannamei) using a 50K SNP chip

Abstract

The objectives of this research were to assess the genetic diversity, population structure, linkage disequilibrium and perform a genome-wide association study (GWAS) to search for single nucleotide polymorphisms (SNPs) that associate with the resistance of Pacific white shrimp (Litopenaeus vannamei) to White Spot Syndrome Virus (WSSV). The line here analyzed was formerly founded with animals originated from different origins (Ecuador, Panama, and United States of America), with a history of resistance to WSSV and they have undergone a selection process, currently reaching up to F6 generation. In a controlled challenge to WSSV, this line showed a binary survival (39.0% ± 1.1%) and time to death (109.7 ± 0.9 h post-infection) (n = 1944). The population was genotyped using a commercially available 50 K SNP chip and ∼32 K SNPs remained after quality control of genotypes. Population structure, extent and decay of linkage disequilibrium (LD), and genetic variability in the population were evaluated. The principal component analysis (PCA) did not show apparent genetic stratification in the population. The LD decay estimated, revealed a rapid decrease in r2 as the physical distance between markers increased. The most significant decrease was observed in the first 30Kb of distance, suggesting the need to use a higher density of informative markers to meet the requirement of a genome-wide association study in L. vannamei. The observed and expected heterozygosities were both = 0.38, which indicates that the population presents acceptable genetic variability for WSSV resistance. Two SNPs were significantly associated to WSSV resistance at a genome-wide level, which in turn together explained 0.17% of the genetic variance for the trait. One identified SNP surpassing the genome-wide significance threshold (chromosome 1 at 51207389 bp) is located near potential candidate genes, such as Arylsulfatase B-like (ARSB), and D-beta-hydroxybutyrate dehydrogenase mitochondrial-like (βhyD); which was linked to the humoral immune response to WSSV, in addition to the Putative mediator of RNA polymerase II transcription subunit 26 (PMed26); which are associated with the hepatopancreas immune response against infection of WSSV and acute hepatopancreatic necrosis disease (AHPND). Our results indicate a polygenic architecture for WSSV resistance in L. vannamei, suggesting that incorporating genome-wide SNP information, through genomic selection, might be the most appropriate approach to accelerate the genetic progress for this trait.