bioRxiv Science⌕ Search

Biology subjects

de Weerd, H. A.

Publications and source records attributed to de Weerd, H. A..

2 recordsLinked to original sources

Representational Learning from Healthy Multi-Tissue Human RNA-seq Data such that Latent Space Arithmetics Extracts Disease Modules

1Developing computational analyses of transcriptomic data has dramatically improved our understanding of complex multifactorial diseases. However, such approaches are limited to small sample sets of disease-affected material, thus being sensitive to statistical biases and noise. Here, we ask if a variational autoencoder (VAE) trained on large groups of healthy, human RNA-seq data of multiple tissues can capture the fundamental healthy gene regulation system such that the learned representation generalizes to account for unseen disease changes. To this end, we trained a multi-scale representation to encode cellular processes ranging from cell types to genegene interactions. Importantly, we found that the learned healthy representations could predict unseen gene expression changes from 25 independent disease datasets. We extracted and decoded disease-specific signals from the VAE latent space to dissect this finding. Interestingly, the gene modules corresponding to this signal contained more disease-specific genes than the respective differential expression analysis in 20 of 25 cases. Finally, we matched genes related to the disease signals to known drug targets. We could extract sets of known and potential pharmaceutical candidates from this analysis and demonstrate the utility in three use cases. In summary, our study showcases how data-driven representation learning using a VAE as a foundational model allows an arithmetic deconstruction of the latent space such that biological insights enable the dissection of disease mechanisms and drug targets. Our model is available at https://github.com/ddeweerd/VAE_Transcriptomics/.

systems biology↗

Systematic GWAS-assessment of disease modules reveals a multi-omic MS module strongly associated with risk factors

BackgroundThere are few (if any) practical guidelines for predictive and falsifiable multi-omics data integration that systematically integrate existing knowledge. Disease modules are popular concepts for interpreting genome-wide studies in medicine but have so far not been systematically evaluated and may lead to corroborating multi-omic modules. MethodsWe assessed eight module identification methods in 57 previously published expression and methylation studies of 19 diseases using GWAS enrichment analysis. Next, we applied the same strategy for multi-omics integration of 19 datasets of multiple sclerosis (MS), and further validated the resulting module using both GWAS and risk-factor associated genes from several independent cohorts. ResultsOur benchmark of modules showed that in immune-associated diseases modules inferred from clique-based methods were the most enriched for GWAS-genes. The multi-omics case study using MS revealed the robust identification of a module of 220 genes. Strikingly, most genes of the module was differentially methylated upon the action of one or several environmental risk factors in MS (n = 217, P = 10-47) and were also independently validated for association with five different risk factors of MS, which further stressed the high genetic and epigenetic relevance of the module for MS. ConclusionWe believe our analysis provides a workflow for selecting modules and our benchmark study may help further improvement of disease module methods. Moreover, we also stress that our methodology is generally applicable for combining and assessing the performance of multi-omics approaches for complex diseases.

bioinformatics↗