bioRxiv Science⌕ Search

bioRxiv · 10.1101/2024.08.31.610262

Fast variance component analysis using large-scale ancestral recombination graphs

Abstract

Recent algorithmic advancements have enabled the inference of genome-wide ancestral recombination graphs (ARGs) from genomic data in large cohorts. These inferred ARGs provide a detailed representation of genealogical relatedness along the genome and have been shown to complement genotype imputation in complex trait analyses by capturing the effects of unobserved genomic variants. An inferred ARG can be used to construct a genetic relatedness matrix, which can be leveraged within a linear mixed model for the analysis of complex traits. However, these analyses are computationally infeasible for large datasets. We introduce a computationally efficient approach, called ARG-RHE, to estimate narrow-sense heritability and perform region-based association testing using an ARG. ARG-RHE leverages a method for computing genotype-matrix products from genealogical data in sublinear time, along with scalable randomized algorithms. This enables fast estimation of variance components and their statistical significance, supports parallel analysis of multiple quantitative traits, and facilitates other linear mixed-model analyses. We conduct extensive simulations to verify the computational efficiency, statistical power, and robustness of this approach. We then apply it to detect associations between 21,159 genes and 52 blood-related traits, using an ARG inferred from genotype data of 337,464 individuals from the UK Biobank. In these analyses, combining ARG-based and imputation-based testing yields 8% more gene-trait associations than using imputation alone, suggesting that inferred genome-wide genealogies may effectively complement genotype imputation in the analysis of complex traits.

Source connections

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Zhu, J., Kalantzis, G., Pazokitoroudi, A., Gunnarsson, A. F., Loya, H., Chen, H., Sankararaman, S., Palamara, P. F.. 2024-08-31. Fast variance component analysis using large-scale ancestral recombination graphs. https://doi.org/10.1101/2024.08.31.610262

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

KEEP EXPLORING

Related preprints

OPA1 controls mitochondrial dysfunction-driven liver fibrosis in MASLD

Progressive hepatic fibrosis is the principal determinant of morbidity and mortality in metabolic dysfunction-associated steatotic liver disease and steatohepatitis (MASLD/MASH). Mitochondrial dysfunction is a hallmark of MASH, and the release of mitochondrial damage-associated molecular patterns (mito-DAMPs) from injured hepatocytes can promote fibrosis. However, how mitochondrial dynamics and quality control shape the fibrotic response in MASLD/MASH remains unclear. Here, through large-scale genomic analyses of mitochondrial genes governing mitophagy, fusion and fission in human MASLD, with a power-equivalent sample size of approximately 700,000 individuals, we identify a strong association between hepatic fibrosis and the mitochondrial fusion factor dynamin-like GTPase optic atrophy 1 (OPA1). OPA1 transcripts and protein abundance in the liver epithelium were progressively dysregulated with advancing fibrosis. In mice, hepatocyte-specific OPA1 loss alone was sufficient to induce hepatic stellate cell activation and fibrosis in zone 3, promoted the release of mito-DAMPs into the circulation and exacerbated fibrosis in experimental MASH. These findings identify OPA1 as a central regulator of the hepatic fibrotic response and connect defective mitochondrial homeostasis to mito-DAMP release, hepatic stellate cell activation and fibrosis in MASLD.

genetics↗

Temporal control of mitochondrial mutagenesis reveals the fate of mtDNA mutations with age

Mutations in the mitochondrial genome (mtDNA) play a critical role in the aging process and a wide variety of age-related diseases. However, it remains unclear when the mutations that drive physiological decline arise. To answer this question, we generated a new mouse model in which mitochondrial mutagenesis can be confined to a defined window of time. Surprisingly, we found that mutations that arise during the first two months of life are sufficient to drive a wide variety of age-related pathologies, and that the severity of this pathology is broadly regulated by distinct, tissue-specific selective pressures that control the fate of mtDNA mutations with age. Further, we found that selection against deleterious variants can be modulated by manipulation of mitochondrial fusion in vitro and in vivo. These observations raise the possibility that in some tissues, the pace of aging is pre-determined by events that occur early in life and that interventions targeting mitochondrial fusion may be able to slow down or reverse the expansion of these pathogenic variants. These results carry far-reaching implications for strategies aimed at preventing or delaying age-related decline.

genetics↗

Innate immune stress pathway activation underlies heterochromatin dysfunction pathology

Heterochromatin loss disrupts nuclear architecture, gene regulation and repetitive element silencing, and is associated with diverse human diseases. However, mechanisms linking heterochromatin dysfunction to pathological phenotypes remain unclear. Using genetic interaction screening and genomic analyses in C. elegans, we identify secondary activation of the Intracellular Pathogen Response (IPR), an innate immune stress pathway, as a major contributor to heterochromatin mutant phenotypes. Constitutive IPR activation phenocopies slow growth and indirect transcriptional changes observed in these mutants. Depletion of genetic enhancers further increased, whereas suppressor RNAi attenuated IPR activation, with direct heterochromatin targets remaining substantially deregulated. Notably, many suppressors encode active chromatin components, and mild reduction of RNA polymerase II activity ameliorates growth defects in C. elegans HP1 mutants and human HP1-deficient cells. Our findings reveal secondary stress response activation as an important mechanism linking heterochromatin dysfunction to pathology and identify transcriptional dampening as a potential therapeutic strategy for mitigating these effects.

genetics↗