Date: 13 January 2026 (Tuesday)
Time: 4:00 pm – 5:00 pm
Venue: Mrs Chen Yang Foo Oi Telemedicine Centre, 2/F, William M.W. Mong Block, 21 Sassoon Road
Host: Professor Michael Hӓusser

Prof. Danny Leung received his BSc in Human Genetics from University College London and his MSc in Human Molecular Genetics from Imperial College London. He completed his PhD under the supervision of Prof. Matthew Lorincz in the Department of Medical Genetics at the University of British Columbia, followed by postdoctoral research with Prof. Bing Ren at the Ludwig Institute for Cancer Research. During this time, he was a California Institute for Regenerative Medicine fellow and served as project manager for the San Diego branch of the NIH Roadmap Epigenomics Project.

Since 2015, Prof. Leung has been a faculty member in the Division of Life Science at the Hong Kong University of Science and Technology (HKUST). His laboratory investigates how epigenetic pathways and nuclear architecture regulate non-coding DNA, with particular emphasis on repetitive elements. He is the Director of the HKUST Center for Epigenomics Research and the lead investigator of the Hong Kong Epigenomics Project.

Prof. Leung has received several distinctions, including the Croucher Innovation Award and Associate Membership at the Ming Wai Lau Centre for Reparative Medicine, and he served as Chair of the 2023 Gordon Research Conference on Genome Architecture in Cell Fate and Disease. His work has been published in leading journals such as Nature, Nature Cell Biology, and PNAS.

Non-coding DNA makes up most of the mammalian genome, yet how it shapes gene activity and cellular identity is only beginning to come into focus. Our research explores how epigenetic regulation and 3D genome architecture work together to interpret this vast non-coding landscape, with particular attention to retrotransposons, abundant repetitive elements that supply a diverse array of regulatory sequences. Across developmental and disease settings, we find that mechanisms such as histone methylation, DNA methylation, and chromatin folding determine when non-coding DNA is activated, silenced, or repurposed. These pathways guide lineage-specific regulatory networks and ensure that retrotransposon-derived enhancers, promoters, and architectural sites are properly controlled. When epigenetic regulation fails, the resulting changes in gene expression and chromatin organization can alter cell identity, disrupt tissue function, and contribute to disease. Overall, our work reveals that repetitive elements are not genomic relics but integral components of gene regulation. By mapping how epigenetic pathways shape non-coding DNA, we aim to uncover core principles that govern development and disease.