ArticleG3 (Bethesda, Md.)2026
Fine mapping and functional annotation of a QTL for resistance to tilapia lake virus in Nile tilapia (Oreochromis niloticus).
Article in G3 (Bethesda, Md.), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
Abstract
Disease resistance is one of the main targets of animal breeding programs. In recent years, incorporating genomic information to accelerate genetic progress has become one of the priorities of the industry. Here, we combined population-scale whole-genome sequencing with differential gene expression and functional annotation analyses to study resistance to tilapia lake virus (TiLV) in a breeding Nile tilapia (Oreochromis niloticus) GIFT population. Fish with survival data from a natural TiLV outbreak were sampled and genotyped for 6.7 M SNPs using whole-genome resequencing and imputation. Our results confirmed a QTL located in the proximal end of Oni22, identifying 74 out of the top 99 markers associated with binary survival within a 10 Mb window. The marker explaining the highest genetic variance of TiLV resistance is located at 1.7 Mb and presents a substitution effect of 0.15. Additionally, other SNPs in several other chromosomes explained a high percentage of the genetic variance, with an important number located in 2 separate regions of Oni09. These results suggest an oligogenic architecture underlying resistance to TiLV, with several QTLs with moderate effect and many with small effect. Host transcriptomic analyses identified genes differentially expressed between resistant and susceptible genotypes according to the QTL in Oni22, highlighting proteosome subunit beta type-9a, and ha1f as potential causal genes. This is the first study combining whole-genome sequencing at a population scale with genomic approaches to assess the underlying genomic basis for TiLV resistance. Our results confirm and narrow down a QTL underlying this key trait in a major aquaculture species worldwide, and found novel QTLs in other chromosomes. The identified markers and genes have the potential to improve resistance to TiLV in Nile tilapia, significantly improving animal health and welfare.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.