Deciphering the regulatory consequences of sequence divergence across human evolution is essential to understanding the molecular basis of human-specific traits and disease. Although millions of derived alleles distinguish humans from great apes, only a small fraction are likely to influence human-specific traits. Previous studies have focused on regions of elevated sequence divergence, assuming that rapid evolution reflects functional adaptation, yet individual high-impact regulatory mutations evade such scans. Here, we apply sequence-to-function deep learning to predict chromatin accessibility across modern human, archaic hominin, and great ape personalized genomes, identifying lineage-specific cis-regulatory elements (linCREs) across diverse cellular contexts. Compared to conserved elements, linCREs are shorter, less pleiotropic, less conserved, and enriched in neurodevelopmental pathways. Many linCREs occur in regions with limited sequence divergence that acceleration-based approaches would overlook. We validate lineage-specific enhancer activity through luciferase reporter assays and demonstrate that a single motif-generating derived allele nominated by model interpretability tools drives a hominin-specific neurodevelopmental enhancer.
Riley J. Mangan, Nikitha Thoduguli, Dimitar Ivanov et al.· bioRxiv· 0 citations
Phenoverse is introduced, an interpretable deep learning framework that learns sample-level disease state representations through cell type-aware residual encoding, prototype learning, and Perceiver-based aggregation that demonstrates that trajectory-derived genes reveal cross-cohort molecular programs and show consistently higher reproducibility than traditional case-control comparisons.
Manoj M Wagle, Yongheng Wang, Soham Samanta et al.· bioRxiv· 0 citations
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