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Biology subjects

Achille, A.

Publications and source records attributed to Achille, A..

3 recordsLinked to original sources

Long-context Protein Language Model

Self-supervised training of language models (LMs) has seen great success for protein sequences in learning meaningful representations and for generative drug design. Most protein LMs are based on the Transformer architecture trained on individual proteins with short context lengths. Such protein LMs cannot extrapolate to longer proteins and protein complexes well. They also fail to account for the underlying biological mechanisms carried out by biomolecular interactions and dynamics i.e., proteins often interact with other proteins, molecules, and pathways in complex biological systems. In this work, we propose LC-PLM based on an alternative protein LM architecture, BiMamba-S, built upon selective structured state-space models, to learn high-quality universal protein representations at the amino acid token level using masked language modeling. We also introduce its graph-contextual variant, LC-PLM-G, which contextualizes protein-protein interaction (PPI) graphs for a second stage of training. LC-PLM demonstrates favorable neural scaling laws, better length extrapolation capability, and up to 30% and 16% improvements on protein downstream tasks compared to Transformer-based ESM-2 when trained with 100B and 1T tokens, respectively. LC-PLM-G further trained within the context of PPI graphs shows promising results on protein structure and function prediction tasks. Our study demonstrates the benefit of increasing the context size with computationally efficient LM architecture (e.g., structured state space models) in learning universal protein representations and incorporating molecular interaction contexts contained in biological graphs.

synthetic biology↗

TLCellClassifier: Machine Learning Based Cell Classification for Bright-Field Time-Lapse Images

Immunotherapies have shown promising results in treating patients with hematological malignancies like multiple myeloma, which is an incurable but treatable bone marrow-resident plasma cell cancer. Choosing the most efficacious treatment for a patient remains a challenge in such cancers. However, pre-clinical assays involving patient-derived tumor cells co-cultured in an ex vivo reconstruction of immune-tumor micro-environment have gained considerable notoriety over the past decade. Such assays can characterize a patients response to several therapeutic agents including immunotherapies in a high-throughput manner, where bright-field images of tumor (target) cells interacting with effector cells (T cells, Natural Killer (NK) cells, and macrophages) are captured once every 30 minutes for upto six days. Cell detection, tracking, and classification of thousands of cells of two or more types in each frame is bound to test the limits of some of the most advanced computer vision tools developed to date and requires a specialized approach. We propose TLCellClassifier (time-lapse cell classifier) for live cell detection, cell tracking, and cell type classification, with enhanced accuracy and efficiency obtained by integrating convolutional neural networks (CNN), metric learning, and long short-term memory (LSTM) networks, respectively. State-of-the-art computer vision software like KTH-SE and YOLOv8 are compared with TLCellClassifier, which shows improved accuracy in detection (CNN) and tracking (metric learning). A two-stage LSTM-based cell type classification method is implemented to distinguish between multiple myeloma (tumor/target) cells and macrophages/monocytes (immune/effector cells). Validation of cell type classification was done both using synthetic datasets and ex vivo experiments involving patient-derived tumor/immune cells. Availability and implementationhttps://github.com/QibingJiang/cell classification ml

cancer biology↗

HDAC11 Deficiency Prevents High-Fat Diet-Induced Obesity and Metabolic Syndrome

Significance StatementObesity is a serious and widespread health problem which has become a growing concern in many societies. Most currently available weight-loss medications do not work for everyone, and the effects decline over time. Thus, there is an urgent need to identify new molecular targets to improve drug development for the treatment of obesity and obesity-related diseases. In this study, we discovered that the histone deacetylase 11 (HDAC11) enzyme is a key regulator of metabolism and obesity, and the absence of HDAC11 prevents obesity in mice. Our findings will facilitate the development of novel therapeutics to treat obesity by targeting HDAC11.\n\nAbstractObesity and its associated metabolic syndromes are the consequence of susceptible genes and obesogenic environments. We report here that histone deacetylase 11 (HDAC11) plays a critical role in the development of obesity and in metabolic homeostasis. HDAC11 knockout mice display resistance to high-fat diet-induced obesity and associated syndromes by enhancing glucose tolerance and insulin sensitivity, attenuating hypercholesterolemia and hyperinsulinemia, and blocking hepatosteatosis and liver damage. Mechanistically, HDAC11 deficiency boosts energy expenditure through promoting thermogenic capacity, which attributes to the elevation of uncoupling protein 1 (UCP1) expression and activity in brown adipose tissue. Moreover, loss of HDAC11 stimulates mitochondrial oxidation, elevates plasma adiponectin, and activates the adiponectin-AdipoR-AMPK pathway in the liver, which may contribute to a reversal in hepatosteatosis. These findings establish HDAC11 as a key regulator of metabolism and indicate that HDAC11 inhibitors may hold promise for treating overweight and obesity-related diseases.

molecular biology↗