Search bioRxiv⌕ Search
Home/Archive/bioRxiv

bioRxiv · 10.1101/2025.02.13.637958

Amoebic gill disease (AGD) in Atlantic Salmon investigated through a holo-omic lens

Thormar, E. A.·Fraslin, C.·Limborg, M. T.·Robledo, D.
View original source ↗Export metadata ↓

Abstract

Interactions between host genetics and the resident microbiota are complex. Understanding these interactions offers interesting alternatives for addressing gill health and disease resistance in salmonids. Amoebic gill disease (AGD), caused by Neoparamoeba perurans, remains a threat to Atlantic salmon, particularly in aquaculture settings where prevention and treatment options are scant. Selective breeding or genetic engineering towards increased AGD resilience present viable prevention strategies. While a number of studies have addressed AGD resistance in Atlantic salmon using transcriptomic and quantitative genetic approaches, the role of the Atlantic salmon gill microbiota in influencing AGD resilience and susceptibility needs further investigation. Addressing this, we leveraged a holo-omic approach using 16S rRNA bacterial profiling, and quantitative genetics, by considering the microbiota as an extended resistance trait of the salmon. We investigated the microbiota of AGD challenged Atlantic salmon in terms of two common resistance indicator traits: gill score and amoebic load. Subsequently we performed a GWAS using both the traditional indicator traits and traits of the microbiota. We found that the gill microbiota of the AGD affected salmon in this study was dominated by two bacterial families Simkaniaceae and Arcobacteracea. We found that microbial diversity and the relative abundance of Simkaniaceae, potentially derived from the amoeba, varied moderately with indicator traits. Additionally we identified several genomic regions that showed suggestive association with gill score and traits of the microbiota, and explored potential candidate genes for AGD resistance. Although much is still unclear regarding gill microbiota dynamics in gill disease, this study highlights the potential of addressing AGD through an integrative approach that considers the interplay between host genetics, the microbiota, and their roles in disease resistance.

Source connections

Explore related subjects

genomicsPreprint

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Thormar, E. A., Fraslin, C., Limborg, M. T., Robledo, D.. 2025-02-18. Amoebic gill disease (AGD) in Atlantic Salmon investigated through a holo-omic lens. https://doi.org/10.1101/2025.02.13.637958

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

bioRxiv2026

Structural variation in repeat elements is widespread in normal human tissues and in tumorigenesis

Somatic mosaicism contributes to genomic variation, yet postzygotic structural variants remain under-characterized. We performed long- and short-read WGS from multiple individuals (n=47 normal tissues; n=168 samples) and identified mosaic structural variants in all individuals and germ layers, impacting a median 285.2 kb/genome. Nearly half of breakpoints were independently validated, with tissue distributions reflecting both early and late developmental origins. Most mosaic variants were repeat-mediated and 8.3% overlapped functional elements, an enrichment compared to germline variants. To extend these analyses in samples where long-read sequencing is infeasible, we measured repeat alterations from short-read sequencing, recapitulating mosaic tissue-specific differences. We characterized tumor- and tissue- specific variation in repeats across 15 cancer types and found tumor-related repeat variation to be similar in scale to that of normal mosaic variation. Tracking repeat changes in cell-free DNA provided a noninvasive approach for tumor monitoring. Our analyses revealed widespread repeat-driven structural variation in health and disease.

genomics↗
bioRxiv2026

RNA isoform-resolved multiplexed sequencing with bioorthogonal barcoding

RNA isoform dysregulation drives disease pathogenesis and is the target of FDA-approved splice-switching therapeutics. However, multiplexed sequencing methods discard splice junction information because only 3' termini are barcoded and counted. Here, we repurpose acylation and click chemistries to conjugate bioorthogonal barcodes (bobcodes) directly onto multiple internal positions along cellular RNAs. Bobcoded RNAs from multiple samples are pooled for multiplexed cDNA synthesis, during which reverse transcriptase switches from each RNA template onto its tethered bobcode with greater than 99% accuracy in species mixing experiments. Bobcode attachment intervals set cDNA insert sizes without a library fragmentation step, and priming with poly(dT) or random hexamers selects between 3'-end counting and full-length isoform capture. A bioorthogonal barcode-sequencing (BOB-seq v0.1) drug screen identifies transcriptome-wide on- and off-target RNA splicing effects and outperforms existing multiplexing RNA sequencing methods in workflow simplicity, sample-to-sample variability, and barcoding accuracy. Bobcodes add isoform resolution to scalable multiplexed RNA sequencing.

genomics↗
bioRxiv2026

Structural polymorphism and population-variable coding capacity of HERV-K(HML-2) in human pangenomes

Approximately 8% of the human genome is derived from ancient retroviral infections. The most recently integrated of these endogenous retroviruses is the HERV-K(HML-2) clade, whose expression has been associated with cancer, amyotrophic lateral sclerosis, and embryogenesis. Studies of HERV expression, particularly HML-2, have relied predominantly on short-read sequencing. However, the high similarity among HML-2 proviruses prevents many short reads from being assigned uniquely to individual loci. We therefore compared haplotype-resolved long-read genome assemblies from 292 donors to resolve variation in proviral structure and coding capacity. Several loci previously thought to be fixed were structurally polymorphic. Tandem arrays occurred at 13 loci and contained up to six proviral copies in a single array. At 8q11.23, we identified a previously undescribed full-length provirus in one haplotype. All 583 other haplotypes carried a solo-LTR. We found that standard reference genomes failed to represent the coding capacity retained in many individuals, whose proviruses contained intact open reading frames despite disruptive mutations in the reference sequences. Short-read genotypes left 32.5% of the tested donor-variant pairs unresolved at sites associated with viral reading frames. These findings show why HML-2 expression must be interpreted in the context of the structural and coding alleles each individual carries.

genomics↗