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Biology subjects

Sudarshan, M.

Publications and source records attributed to Sudarshan, M..

3 recordsLinked to original sources

Machine learning for discovery: deciphering RNA splicing logic

Machine learning methods, particularly neural networks trained on large datasets, are transforming how scientists approach scientific discovery and experimental design. However, current state-of-the-art neural networks are limited by their uninterpretability: despite their excellent accuracy, they cannot describe how they arrived at their predictions. Here, using an "interpretable-by-design" approach, we present a neural network model that provides insights into RNA splicing, a fundamental process in the transfer of genomic information into functional biochemical products. Although we designed our model to emphasize interpretability, its predictive accuracy is on par with state-of-the-art models. To demonstrate the models interpretability, we introduce a visualization that, for any given exon, allows us to trace and quantify the entire decision process from input sequence to output splicing prediction. Importantly, the model revealed novel components of the splicing logic, which we experimentally validated. This study highlights how interpretable machine learning can advance scientific discovery.

molecular biology↗

Fast Kernel-based Association Testing of non-linear genetic effects for Biobank-scale data

Our knowledge of non-linear genetic effects on complex traits remains limited, in part, due to the modest power to detect such effects. While kernel-based tests offer a powerful approach to test for nonlinear relationships between sets of genetic variants and traits, current approaches cannot be applied to Biobank-scale datasets containing hundreds of thousands of individuals. We propose, FastKAST, a Kernel-based approach that can test for non-linear effects of a set of variants on a trait. FastKAST provides calibrated hypothesis tests while enabling analysis of Biobank-scale datasets with hundreds of thousands of individuals. We applied FastKAST to thirty quantitative traits measured across {approx} 300 K unrelated white British individuals in the UK Biobank to detect sets of variants with nonlinear effects at genome-wide significance.

genetics↗

14-3-3γ prevents centrosome duplication by inhibiting NPM1 function.

14-3-3 proteins bind to ligands via phospho-Serine containing consensus motifs. However, the molecular mechanisms underlying complex formation and dissociation between 14-3-3 proteins and their ligands remain unclear. We identified two conserved acidic residues in the 14-3-3 peptide-binding pocket (D129 and E136) that potentially regulate complex formation and dissociation. Altering these residues to Alanine led to opposing effects on centrosome duplication. D129A inhibited centrosome duplication while E136A stimulated centrosome amplification. These results were due to the differing abilities of these mutant proteins to form a complex with NPM1. Inhibiting complex formation between NPM1 and 14-3-3{gamma} led to an increase in centrosome duplication and overrode the ability of D129A to inhibit centrosome duplication. We identify a novel role of 14-3-3 in regulating centrosome licensing and a novel mechanism underlying the formation and dissociation of 14-3-3 ligand complexes dictated by conserved residues in the 14-3-3 family.

cell biology↗