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Wu, A. P.

Publications and source records attributed to Wu, A. P..

2 recordsLinked to original sources

Virtual phenotypic screening discovers novel scaffolds inhibiting the PI3K/mTOR pathway

Phenotypic drug discovery has yielded many first-in-class small-molecule drugs by discovering modulators of disease phenotypes in physiologically relevant cellular systems. However, high-content phenotypic assays lack the ultra-high-throughput scalability of target-based screens. Recent advances in virtual screening present an opportunity to address this bottleneck, but have been limited to simple phenotypes like viability, restricted to small repurposing libraries, or lack in-depth biological validation. Here, we present PhenoCompass, a multimodal co-embedding model that aligns compound structures and high-content phenotypic imaging to enable virtual phenotypic screening over billion-compound libraries. Following training on the Joint Undertaking in Morphology dataset with more than 100,000 Cell Painting compound profiles, retrospective validation with historical biochemical high-throughput screening data demonstrates that PhenoCompass ranks compounds according to their biochemical target engagement. Leveraging PhenoCompass, we performed a prospective screen of 3.8 billion Enamine REAL compounds for inhibitors of PI3K/mTOR pathway, a critical signaling cascade whose aberrant activation is a common tumor driver. This search identified 11 novel compounds with pathway-consistent Cell Painting readout and diverse scaffolds, a 54-fold enrichment over the training set. Orthogonal validation experiments using a FOXO3A reporter assay and direct kinase inhibition confirmed seven structurally novel inhibitors with distinct mechanisms of action. These results highlight the convergence of diverse molecular target profiles onto a shared morphological pathway signature and establish PhenoCompass as a robust framework for high-content phenotypic virtual screening.

bioinformatics↗

Unraveling causal gene regulation from the RNA velocity graph using Velorama

Single-cell expression dynamics from differentiation trajectories or RNA velocity have the potential to reveal causal links between transcription factors (TFs) and their target genes in gene regulatory networks (GRNs). However, existing methods either neglect these expression dynamics or require cells to be ordered along a linear pseudotemporal axis, which is incompatible with branching trajectories. We introduce Velorama, an approach to causal GRN inference that represents single-cell differentiation dynamics as a directed acyclic graph (DAG) of cells constructed from pseudotime or RNA velocity measurements. In contrast to previous approaches, Velorama is able to work directly with RNA velocity-based cell-to-cell transition probabilities and enables estimates of TF interaction speeds with their target genes. On a set of synthetic datasets, Velorama substantially outperforms existing approaches, improving area under the precision-recall curve (AUPRC) by 3.7-4.8x over the next best method. Applying Velorama to four RNA velocity datasets, we uncover evidence that the speed of a TFs interactions is tied to its regulatory function. For human corticogenesis, we find slow TFs to be linked to gliomas and co-regulate preferentially with fast TFs, while fast TFs are associated with neuropsychiatric diseases. We expect Velorama to be a critical part of the RNA velocity toolkit for investigating the causal drivers of differentiation and disease. Software availabilityhttps://cb.csail.mit.edu/cb/velorama

bioinformatics↗