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This study applies fine-tuned DNABERT deep learning models to predict the functional impact of non-coding variants in human gene regulatory regions, addressing a critical gap beyond standard coding-sequence analysis. By integrating attention-based motif disruption detection with clinical survival data from glioblastoma samples, the framework links specific genomic alterations directly to patient outcomes. The work demonstrates how advanced machine learning architectures can effectively prioritize clinically relevant mutations previously obscured by complex non-coding DNA landscapes.
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DeepVRegulome: DNABERT-based deep-learning framework for predicting the functional impact of short genomic variants on the human regulome

arXiv2 min read

arXiv:2511.09026v2 Announce Type: replace-cross Abstract: Whole-genome sequencing (WGS) has revealed numerous non-coding short variants whose functional impacts remain poorly understood. Despite recent advances in deep-learning genomic approaches, accurately predicting and prioritizing clinically relevant mutations in gene regulatory regions remains a major challenge. We developed DeepVRegulome, a computational framework integrating 464 fine-tuned DNABERT models (458 transcription factor, 4 histone mark, and 2 splice site models) trained on ENCODE and GENCODE datasets. The framework pairs these deep learning models with a suite of analytical tools: quantitative variant scoring via log-odds ratios to assess functional impact, attention-based motif analysis to identify disrupted sequence patterns, and survival analysis using Kaplan-Meier and Cox proportional hazards models to link high-impact variants with clinical outcomes. To ensure the framework accurately captures variant effects on baseline binding status, we benchmarked DeepVRegulome against an independent experimental assay of allele-specific transcription factor binding (SNP-SELEX) data and compared its performance to four established variant-effect predictors. The analysis identified 572 splice-disrupting and 9,837 transcription-factor binding site-altering mutations occurring in greater than 10 percentage of glioblastoma samples. Survival analysis linked 1352 mutations and 563 disrupted regulatory regions to patient outcomes, enabling stratification via non-coding mutation signatures. All the code, fine-tuned models, and an interactive data portal are publicly available.

Abstract:Whole-genome sequencing (WGS) has revealed numerous non-coding short variants whose functional impacts remain poorly understood. Despite recent advances in deep-learning genomic approaches, accurately predicting and prioritizing clinically relevant mutations in gene regulatory regions remains a major challenge. We developed DeepVRegulome, a computational framework integrating 464 fine-tuned DNABERT models (458 transcription factor, 4 histone mark, and 2 splice site models) trained on ENCODE and GENCODE datasets. The framework pairs these deep learning models with a suite of analytical tools: quantitative variant scoring via log-odds ratios to assess functional impact, attention-based motif analysis to identify disrupted sequence patterns, and survival analysis using Kaplan-Meier and Cox proportional hazards models to link high-impact variants with clinical outcomes. To ensure the framework accurately captures variant effects on baseline binding status, we benchmarked DeepVRegulome against an independent experimental assay of allele-specific transcription factor binding (SNP-SELEX) data and compared its performance to four established variant-effect predictors. The analysis identified 572 splice-disrupting and 9,837 transcription-factor binding site-altering mutations occurring in greater than 10 percentage of glioblastoma samples. Survival analysis linked 1352 mutations and 563 disrupted regulatory regions to patient outcomes, enabling stratification via non-coding mutation signatures. All the code, fine-tuned models, and an interactive data portal are publicly available.

Genomics (q-bio.GN); Artificial Intelligence (cs.AI); Machine Learning (cs.LG)

arXiv:2511.09026 [q-bio.GN]

(or arXiv:2511.09026v2 [q-bio.GN] for this version)

Full text under the publisher's open licence · 217 words

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