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Image-based profiling has emerged as a powerful technology for various steps in basic biological and pharmaceutical discovery, but the community has lacked a large, public reference set of data from chemical and genetic perturbations. Here we present data generated by the Joint Undertaking for Morphological Profiling (JUMP)-Cell Painting Consortium, a collaboration between 10 pharmaceutical companies, six supporting technology companies, and two non-profit partners. When completed, the dataset will contain images and profiles from the Cell Painting assay for over 116,750 unique compounds, over-expression of 12,602 genes, and knockout of 7,975 genes using CRISPR-Cas9, all in human osteosarcoma cells (U2OS). The dataset is estimated to be 115 TB in size and capturing 1.6 billion cells and their single-cell profiles. File quality control and upload is underway and will be completed over the coming months at the Cell Painting Gallery:https://registry.opendata.aws/cellpainting-gallery. A portal to visualize a subset of the data is available athttps://phenaid.ardigen.com/jumpcpexplorer/.

International audience; With the automation of biological experiments and the increase of quality of single cell data that can now be obtained by phospho-proteomic and time lapse videomicroscopy, automating the building of mechanistic models from these data time series becomes conceivable and a necessity for many new applications. While learning numerical parameters to fit a given model structure to observed data is now a quite well understood subject, learning the structure of the model is a more challenging problem that previous attempts failed to solve without relying quite heavily on prior knowledge about that structure. In this paper, we consider mechanistic models based on chemical reaction networks (CRN) with their continuous dynamics based on ordinary differential equations, and finite time series about the time evolution of concentration of molecular species for a given time horizon and a finite set of perturbed initial conditions. We present a greedy heuristics unsupervised statistical learning algorithm to infer reactions with a time complexity for inferring one reaction in O(t.n 2) where n is the number of species and t the number of observed transitions in the traces. We evaluate this algorithm both on simulated data from hidden CRNs, and on real videomicroscopy single cell data about the circadian clock and cell cycle progression of NIH3T3 embryonic fibroblasts. In all cases, our algorithm is able to infer meaningful reactions, though generally not a complete set for instance in presence of multiple time scales or highly variable traces.

International audience; With the automation of biological experiments and the increase of quality of single cell data that can now be obtained by phosphoproteomic and time lapse videomicroscopy, automating the building of mechanistic models from these time series data becomes conceivable and a necessity for many new applications. While learning numerical parameters to fit a given model structure to observed data is now a quite well understood subject, learning the structure of the model is a more challenging problem that previous attempts failed to solve without relying quite heavily on prior knowledge about that structure. In this paper , we consider mechanistic models based on chemical reaction networks (CRN) with their continuous dynamics based on ordinary differential equations, and finite time series about the time evolution of concentration of molecular species for a given time horizon and a finite set of perturbed initial conditions. We present a statistical learning algorithm to learn CRNs with a time complexity for inferring one reaction in O(t.n 2) where n is the number of species and t the number of observed transitions in the traces. We learn both the structure and the reaction rates of the CRN. We evaluate this algorithm and its sensitivity to its statistical threshold parameters, first on simulated data from a hidden CRN, and second on real videomicroscopy single cell time series data over three days about the circadian clock and cell cycle progression of NIH3T3 embryonic fi-broblasts. In all cases, our algorithm is able to reconstruct meaningful CRNs. We discuss some limits according to the existence of multiple time scales and highly variable traces.