Portrait of Jun Ding

Jun Ding

Affiliate Member
Assistant professor, McGill University, Department of Medicine
Research Topics
Computational Biology
Medical Machine Learning
Representation Learning
Website
Google Scholar

Biography

Jun Ding is an assistant professor in the Department of Medicine of the Faculty of Medicine and Health Sciences at McGill University.

Alongside his team, he is dedicated to employing machine learning techniques to decipher the complex dynamics of cells in various diseases, such as developmental disorders, pulmonary diseases and cancers. The diverse and intricate nature of these conditions necessitates innovative approaches, prompting the use of state-of-the-art single-cell technologies to meticulously profile individual cell states. The result is a rich source of data for our machine learning models.

These technologies present unprecedented opportunities to advance understanding, particularly in fields like developmental and cancer biology. However, the challenge is to develop computational models capable of linking this intricate biomedical data to potential discoveries.

Ding’s primary focus lies in the development and refinement of machine learning methodologies, especially probabilistic graphical models, to effectively analyze, model and visualize both single-cell and bulk omics data, often featuring longitudinal or spatial dimensions. The goal is to harness these advanced machine learning techniques to deepen the comprehension of cellular dynamics, and so develop groundbreaking diagnostic and therapeutic strategies that can significantly benefit public health.

Current Students

Vishvak Raghavan
Master's Research - McGill University
Principal supervisor :
Yue Li
Github

Publications

Inhibition of epithelial cell YAP-TEAD/LOX signaling attenuates pulmonary fibrosis in preclinical models
Darcy Elizabeth Wagner
Hani N. Alsafadi
Nilay Mitash
Aurelien Justet
Qianjiang Hu
Ricardo Pineda
Claudia Staab-Weijnitz
Martina Korfei
Nika Gvazava
Kristin Wannemo
Ugochi Onwuka
Molly Mozurak
Adriana Estrada-Bernal
Juan Cala Garcia
Katrin Mutze
Rita Costa
Deniz Bölükbas
John Stegmayr
Wioletta Skronska-Wasek
Stephan Klee … (see 14 more)
Chiharu Ota
Hoeke A. Baarsma
Jingtao Wang
John Sembrat
Anne Hilgendorff
Jun Ding
Andreas Günther
Rachel Chambers
Ivan O Rosas
Stijn de Langhe
Naftali Kaminski
Mareike Lehmann
Oliver Eickelberg
Melanie Königshoff
Idiopathic pulmonary fibrosis (IPF) is a progressive and lethal disease characterized by excessive extracellular matrix deposition. Current … (see more)IPF therapies slow disease progression but do not stop or reverse it. The (myo)fibroblasts are thought to be the main cellular contributors to excessive extracellular matrix production in IPF. Here we show that fibrotic alveolar type II cells regulate production and crosslinking of extracellular matrix via the co-transcriptional activator YAP. YAP leads to increased expression of Lysl oxidase (LOX) and subsequent LOX-mediated crosslinking by fibrotic alveolar type II cells. Pharmacological YAP inhibition via verteporfin reverses fibrotic alveolar type II cell reprogramming and LOX expression in experimental lung fibrosis in vivo and in human fibrotic tissue ex vivo. We thus identify YAP-TEAD/LOX inhibition in alveolar type II cells as a promising potential therapy for IPF patients.
2025-08-02
Nature Communications (published)
doi.org
DOLPHIN advances single-cell transcriptomics beyond gene level by leveraging exon and junction reads
Kailu Song
Yumin Zheng
Bowen Zhao
David H. Eidelman
Jian Tang
Jun Ding
2025-07-04
Nature Communications (published)
doi.org
Harnessing agent-based frameworks in CellAgentChat to unravel cell-cell interactions from single-cell and spatial transcriptomics
Vishvak Raghavan
Yumin Zheng
Yue Li
Jun Ding
2025-07-01
Genome Research (published)
doi.org
Alveolar epithelial cell plasticity and injury memory in human pulmonary fibrosis
Taylor S Adams
Jonas C Schupp
Agshin Balayev
Johad Khoury
Aurelien Justet
Fadi Nikola
Laurens J De Sadeleer
De Sadeleer J Laurens
Juan Cala Garcia
Marta Zapata-Ortega
Panayiotis V Benos
Benos V Panayiotis
P.V. Benos
John E McDonough
Farida Ahangari
Melanie Königshoff
Jun Ding
Robert J Homer
Ivan O Rosas
Xiting Yan … (see 3 more)
Bart M Vanaudenaerde
Wim A Wuyts
Naftali Kaminski
2025-06-21
bioRxiv (preprint)
doi.org
A deep generative model for deciphering cellular dynamics and in silico drug discovery in complex diseases.
Yumin Zheng
Jonas C Schupp
Taylor S Adams
Geremy Clair
Aurelien Justet
Farida Ahangari
Xiting Yan
Paul Hansen
Marianne Carlon
Emanuela Cortesi
Marie Vermant
Robin Vos
De Sadeleer J Laurens
Ivan O Rosas
Ricardo Pineda
John Sembrat
Melanie Königshoff
John E McDonough
Bart M. Vanaudenaerde
Wim A Wuyts … (see 2 more)
Naftali Kaminski
Jun Ding
2025-06-20
Nature Biomedical Engineering (published)
doi.org
Advancing global antifungal development to combat invasive fungal infection
Xiu-Li Wang
Jun Ding
Koon Ho Wong
Chen Ding
Chang-Bin Chen
Wen-Juan Wu
Ningning Liu
2025-06-01
hLife (published)
doi.org
DTractor enhances cell type deconvolution in spatial transcriptomics by integrating deep neural networks, transfer learning, and matrix factorization
Yong Jin Kweon
Chenyu Liu
Gregory Fonseca
Jun Ding
2025-04-18
bioRxiv (preprint)
doi.org
Efficient and scalable construction of clinical variable networks for complex diseases with RAMEN.
Yiwei Xiong
Jingtao Wang
Xiaoxiao Shang
Tingting Chen
Douglas D. Fraser
Gregory Fonseca
Simon Rousseau
Jun Ding
2025-04-01
Cell Reports Methods (published)
doi.org
scCobra allows contrastive cell embedding learning with domain adaptation for single cell data integration and harmonization
Bowen Zhao
Kailu Song
Dong-Qing Wei
Yi Xiong
Jun Ding
2025-02-13
Communications Biology (published)
doi.org
DTPSP: A Deep Learning Framework for Optimized Time Point Selection in Time-Series Single-Cell Studies
Michel Hijazin
Pumeng Shi
Jingtao Wang
Jun Ding
2024-12-20
bioRxiv (preprint)
doi.org
DTPSP: A Deep Learning Framework for Optimized Time Point Selection in Time-Series Single-Cell Studies
Michel Hijazin
Pumeng Shi
Jingtao Wang
Jun Ding
Time-series studies are critical for uncovering dynamic biological processes, but achieving comprehensive profiling and resolution across mu… (see more)ltiple time points and modalities (multi-omics) remains challenging due to cost and scalability constraints. Current methods for studying temporal dynamics, whether at the bulk or single-cell level, often require extensive sampling, making it impractical to deeply profile all time points and modalities. To overcome these limitations, we present DTPSP, a deep learning framework designed to identify the most informative time points in any time-series study, enabling resource-efficient and targeted analyses. DTPSP models temporal gene expression patterns using readily obtainable data, such as bulk RNA-seq, to select time points that capture key system dynamics. It also integrates a deep generative module to infer data for non-sampled time points based on the selected time points, reconstructing the full temporal trajectory. This dual capability enables DTPSP to prioritize key time points for in-depth profiling, such as single-cell sequencing or multi-omics analyses, while filling gaps in the temporal landscape with high fidelity. We apply DTPSP to developmental and disease-associated time courses, demonstrating its ability to optimize experimental designs across bulk and single-cell studies. By reducing costs, enabling strategic multi-omics profiling, and enhancing biological insights, DTPSP provides a scalable and generalized solution for investigating dynamic systems.
2024-12-20
bioRxiv (preprint)
doi.org
CellSexID: Sex-Based Computational Tracking of Cellular Origins in Chimeric Models
Huilin Tai
Qian Li
Jingtao Wang
Jiahui Tan
Ryann Lang
Basil J. Petrof
Jun Ding
Cell tracking in chimeric models is essential yet challenging, particularly in developmental biology, regenerative medicine, and transplanta… (see more)tion studies. Existing methods, such as fluorescent labeling and genetic barcoding, are technically demanding, costly, and often impractical for dynamic, heterogeneous tissues. To address these limitations, we propose a computational framework that leverages sex as a surrogate marker for cell tracking. Our approach uses a machine learning model trained on single-cell transcriptomic data to predict cell sex with high accuracy, enabling clear distinction between donor (male) and recipient (female) cells in sex-mismatched chimeric models. The model identifies specific genes critical for sex prediction and has been validated using public datasets and experimental flow sorting, confirming the biological relevance of the identified cell populations. Applied to skeletal muscle macrophages, our method revealed distinct transcriptional profiles associated with cellular origins. This pipeline offers a robust, cost-effective solution for cell tracking in chimeric models, advancing research in regenerative medicine and immunology by providing precise insights into cellular origins and therapeutic outcomes.
2024-12-05
bioRxiv (preprint)
doi.org