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Catona, O.

Publications and source records attributed to Catona, O..

2 recordsLinked to original sources

Coordinate- and Sequence-Based Features for a new Combined Annotation-Dependent Depletion Framework of Structural Variants (CADD-SV v2.0)

Structural variants are a major source of genomic variation and contribute to human disease and evolution through diverse mechanisms, yet their functional interpretation remains challenging. We present CADD-SV v2.0, an improved machine learning framework for scoring SV deleteriousness that expands on the original CADD-SV implementation. This version introduces a unified Random Forest model trained on an expanded set of proxy-neutral and proxy-deleterious variants drawn from human and non-human primate genomes. The model integrates updated genomic annotations, including constraint metrics, regulatory elements, and chromatin architecture features. It scores Deletions, Insertions, Duplications and Inversions based on a single scoring framework that uses both the variant and its flanking regions. To complement this framework, we also explore sequence-based annotations derived from SegmentNT, a deep learning model that provides functional predictions from DNA sequence at nucleotide resolution. Our analysis evaluated whether sequence-derived functional signals can provide additional information for SV prioritization and whether additional models with these features alone or in combination with previous coordinate-based annotations can be used.\ CADD-SV v2.0 outperforms its previous version and other tools in prioritizing deleterious variants across major SV types, including some previously unsupported, and substantially improves the computational workflow, increasing predictive power for genome-wide SV interpretation.

bioinformatics↗

Bridging between mouse and human enhancer-promoter long-range interactions in neural stem cells, to understand enhancer function in neurodevelopmental disease

Non-coding variation in complex human disease has been well established by genome-wide association studies, and it is thought to involve regulatory elements, such as enhancers, whose variation affects the expression of the gene responsible for the disease. The regulatory elements often lie far from the gene they regulate, or within introns of genes differing from the regulated gene, making it difficult to identify the gene whose function is affected by a given enhancer variation. Enhancers are connected to their target gene promoters via long-range physical interactions (loops). In our study, we re-mapped, onto the human genome, more than 10,000 enhancers connected to promoters via long-range interactions, that we had previously identified in mouse brain-derived neural stem cells by RNApolII-ChIA-PET analysis, coupled to ChIP-seq mapping of DNA/chromatin regions carrying epigenetic enhancer marks. These interactions are thought to be functionally relevant. We discovered, in the human genome, thousands of DNA regions syntenic with the interacting mouse DNA regions (enhancers+connected promoters). We further annotated these human regions regarding their overlap with sequence variants (single nucleotide polymorphisms, SNPs; copy number variants, CNVs), that were previously associated with neurodevelopmental disease in human. We document various cases in which the genetic variant, associated in human to neurodevelopmental disease, affects an enhancer involved in long-range interactions: SNPs, previously identified by genome-wide association studies to be associated with schizophrenia, bipolar disorder, and intelligence, are located within our human syntenic enhancers, and alter transcription factors recognition sites. Similarly, CNVs associated to autism spectrum disease and other neurodevelopmental disorders overlap with our human syntenic enhancers. Some of these enhancers are connected (in mouse) to homologs of genes already associated to the human disease, strengthening the hypothesis that the gene is indeed involved in the disease. Other enhancers are connected to genes not previously associated with the disease, pointing to their possible pathogenetic involvement. Our observations provide a resource for further exploration of neural disease, in parallel with the now widespread genome-wide identification of DNA variants in patients with neural disease.

neuroscience↗