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| Main Authors: | , , , , , , , , , , |
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| Format: | Artículo científico |
| Language: | en |
| Published: |
BMC genomics
2026
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| Online Access: | https://pubmed.ncbi.nlm.nih.gov/42298410/ |
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Table of Contents:
- Moderate-high heritability and QTL associated with Manila clam Ruditapes philippinarum resistance to the parasite Perkinsus olseni. Sambade, I M Cao, A Costas, D de Santiago, J A Ortega-Iñarrea, M Hermida, M Pardo, B G Caballero, A Gallo, M Villalba, A Martínez, P The Manila clam (Ruditapes philippinarum) is one of the most valuable bivalves in global aquaculture, but its production is increasingly threatened by Perkinsus olseni, a protozoan parasite responsible for severe mortality events on shellfish beds. Understanding the genetic basis of resistance to this pathogen is essential for developing sustainable breeding strategies and reducing economic losses. We conducted a genome-wide association study (GWAS) on 606 Manila clam offspring from 32 full-sib families to investigate the heritability and genomic architecture of resistance to P. olseni. Following quality control and exclusion of the 42 smallest individuals potentially affected by size-related exposure bias, 564 offspring were retained for the final GWAS analyses. Genomic screening was performed with a newly developed multispecies SNP array comprising 49,392 SNPs for R. philippinarum. Experimental challenges were carried out in two tanks (challenged and control), each containing 1,500 offspring, and parasite load was quantified by qPCR using control Ct values as a non-infected reference. A substantial proportion of phenotypic variation in parasite load was explained by additive genetic effects, with heritability estimated at h² = 0.45 ± 0.09 using the full dataset and increasing to h² = 0.53 ± 0.08 after filtering. Several genome-wide significant quantitative trait loci (QTL) were identified across seven chromosomes, supporting a polygenic basis for resistance. Notably, one QTL on chromosome 18 also showed a highly significant association within one of the largest families. Patterns of linkage disequilibrium (LD) revealed rapid decay across most chromosomes, typical of marine bivalves, except for three chromosomes showing extended LD patterns compatible with putative structural polymorphisms, including possible inversions. These results demonstrate a substantial additive genetic component underlying resistance to P. olseni in Manila clam and highlight chromosome 18 as an important genomic region associated with parasite burden. Overall, our findings support the future integration of genomic tools into selective breeding programmes aimed at improving disease resilience and promoting the long-term sustainability of Manila clam aquaculture under increasing environmental and pathogen pressures.