Search bioRxiv⌕ Search

bioRxiv · 10.64898/2026.06.11.731523

Trustworthy agentic genomics through versioned skill libraries

Abstract

Genomics is adopting autonomous AI agents that interpret genomes from natural-language instructions faster than it is building the means to trust them. We report the first large-scale controlled evaluation of where, in an agentic genomic pipeline, correctness must reside for the system to be trustworthy at clinical scale. Using pharmacogenomics, a domain where errors are measurable and sometimes lethal, we benchmarked nine frontier large language models across 44,550 scored evaluations on 110 pharmacogenomic cases, and tested model interpretation of real star-allele diplotypes from more than 7,000 individuals in three ancestrally diverse populations. Trustworthiness proved to be a property of pipeline architecture, not of the model. Letting the model reason was stochastic and unsafe, and grounding it in the correct guidelines by retrieval paradoxically increased lethal-class errors. Encoding the validated decision logic as a versioned skill and executing it as code made the pharmacogenomic mapping exact, auditable and identical across models, confining all residual error to a single input-interpretation step. On individual genomes, unguarded model interpretation degraded along an ancestry gradient; execution removes this gradient from the clinical mapping, relocating it to the auditable completeness of the input caller. This establishes a generalisable, auditable architecture for trustworthy agentic genome interpretation at scale. HighlightsO_LICorrectness must be executed, not reasoned or retrieved, to be trustworthy C_LIO_LIRetrieval raises phenotype accuracy yet increases lethal-class errors; skills do not C_LIO_LIExecution makes the clinical mapping exact and model-invariant; error stays at input C_LIO_LIA deterministic input caller is the predicted route to all-correct emitted answers C_LI In briefCorpas and colleagues show that trustworthy agentic genome interpretation comes not from making language models reason correctly about biology, but from confining them to interpreting input while versioned, validated skills do the reasoning as executed code. Across nine large language models and 110 pharmacogenomics cases, executing the skill makes the clinical mapping deterministic, auditable and model-invariant. SignificanceGenomics is adopting autonomous, language-model-mediated agents faster than it is building the standards needed to trust them. On a pharmacogenomic benchmark with lethal-class consequences, we show that an agents trustworthiness is not a property of the model but of how the agent is constrained: correctness must be moved out of the stochastic model into a versioned skill executed as code, with the model confined to interpreting heterogeneous input. This gives the field a transferable architecture for trustworthy agentic genome interpretation, a predicted route to deploying it so that every emitted answer is correct (execute the validated skill, call the input deterministically, and abstain on the irreducible residual), and a way to develop genomic skills as validated, executable, versioned units rather than prompts. Following a validation framework described elsewhere, we use clinical-grade to mean determinism, auditability, traceability to versioned components and population-invariant performance, all achieved under skill-constrained execution. We distinguish two senses of population performance: the executed clinical mapping is population-invariant by construction, verified across European, Latin American and East African origin individuals, whereas the models interpretation of real, ancestrally diverse diplotypes is not, degrading along an ancestry gradient, which is precisely why the mapping must be executed rather than reasoned. We do not claim full clinical validation, which would additionally require non-canonical inputs, real-world genomic and clinical data, human comparators and multi-site concordance.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Corpas, M., Iacoangeli, A., Bourdenx, M., Aldraimli, M., Skene, N., Fatumo, S., Guio, H.. 2026-06-15. Trustworthy agentic genomics through versioned skill libraries. https://doi.org/10.64898/2026.06.11.731523

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

KEEP EXPLORING

Related preprints

Chromosome-level, haplotype-resolved genome assembly of the tanniferous forage legume big trefoil (Lotus pedunculatus Cav.) using CiFi

Big trefoil (Lotus pedunculatus Cav.) is a perennial forage legume that thrives on acidic, low-fertility soils and produces condensed tannins that reduce enteric methanogenesis in ruminants. Despite this agronomic potential, genomic resources for the species remain scarce, and the existing haploid assembly does not resolve the two haplotypes of this outcrossing diploid species. Here we present a haplotype-resolved, chromosome-level reference genome for L. pedunculatus genotype Lusitano29 -- the first plant genome assembled using CiFi, a long-read chromosome conformation capture method. We combined PacBio HiFi long reads with CiFi concatemers produced from DpnII and HindIII libraries; in silico digestion and combinatorial pairing of the resulting monomers yielded 790.3 M and 10.3 M pseudo-paired contacts, respectively, enabling scaffolding and manual curation to chromosome level. The 991.1 Mb assembly resolves two phased haplotypes of 500 and 491 Mb, with 96.6% of the sequence anchored in twelve pseudo-chromosomes (six per haplotype). Telomeric repeats were detected at 19 of 24 pseudo-chromosome ends, and no structural errors were detected (scaffold N50 73.8 Mb; consensus QV 64.7; k-mer completeness 99.4%; genome-mode BUSCO completeness 97.0%; CRAQ S-AQI 100.0). Annotation supported by PacBio Iso-Seq full-length transcripts predicted 38,069 and 36,484 protein-coding genes in haplotypes 1 and 2, respectively (protein-mode BUSCO completeness 96.5%), indicating a high completeness of annotated genes. This genome assembly provides a foundation for allele-aware trait dissection of proanthocyanidin biosynthesis, comparative genomics in Lotus, and population genomics and genomics-assisted breeding in L. pedunculatus.

genomics↗

Bramble: projection of spliced genomic alignments into transcriptomic space for improved transcript quantification

Accurate transcript abundance estimation is central to many transcriptomic studies. Many current quantification methods rely on reads mapped directly to the transcriptome, but transcriptome alignment can misassign reads from unannotated transcripts to annotated isoforms, leading to biased abundance estimates. We introduce Bramble, a method that projects spliced genomic alignments into transcriptomic coordinates to produce alignments compatible with downstream transcript quantification tools. Across simulated short- and long-read RNA-seq datasets and multiple levels of reference annotation completeness, incorporating Bramble into quantification pipelines consistently improved accuracy and reduced error. These results suggest that genome-derived transcriptomic alignments can improve transcript quantification by preserving compatible alignments to annotated transcripts while filtering alignments likely originating from unannotated transcripts.

genomics↗

PRDM9-mediated meiotic hotspot specification is constrained in humans despite extensive sequence diversity

PRDM9 specifies meiotic recombination hotspots through a rapidly evolving C2H2 zinc-finger (ZNF) coding minisatellite that determines DNA-binding specificity. Although this minisatellite harbors extraordinary allelic diversity in humans, the functional consequences of most naturally occurring variants remain unknown. Here we functionally characterize 80 human PRDM9 alleles using genome-wide chromatin profiling. Despite extensive sequence diversity within the ZNF array, most alleles function indistinguishably from common A and C hotspot-specifying alleles, revealing that human PRDM9 function is more constrained than its sequence diversity predicts. In contrast, rare and infertility-associated variants occupy two functional extremes: either abundant and novel DNA binding specificity or minimal DNA binding, suggesting that both gain- and loss-of-function alleles may disrupt symmetric hotspot specification during meiosis, thus representing a plausible contributor to human infertility. Together, our findings define the functional landscape of human PRDM9 variation and provide a framework for interpreting the impact of newly discovered PRDM9 alleles.

genomics↗