Date: 16 November 2026 (Monday)
Time: 4:00 pm – 5:00 pm
Venue: Seminar Room 304, 3/F, William M.W. Mong Block, 21 Sassoon Road 
Host: Professor Mu He

Dr. Jinghua Hu is a Professor of Biochemistry and Molecular Biology and Professor of Medicine at Mayo Clinic. He leads the Cilia and Ciliopathies Laboratory and serves as Director of the Model Organism Core at the Robert M. and Billie Kelley Pirnie Translational PKD Center. His laboratory investigates the fundamental biology of primary cilia and the molecular mechanisms underlying human ciliopathies, using an integrated research platform that spans model organisms, mammalian disease models, and human patient-derived samples.

Dr. Hu’s research has made important contributions to understanding ciliogenesis and ciliary gating. His group was the first to demonstrate that transition fibers at the ciliary base constitute a key component of the ciliary gate，controlling the selective entry of membrane and soluble proteins into cilia. His laboratory has also advanced the understanding of ciliopathy-associated genes, post-translational modifications of ciliary microtubules, selective trafficking of sensory receptors and signaling molecules, and the regulation of cilia-dependent signaling pathways. His disease-focused research encompasses inherited ciliopathies, including Joubert syndrome, Bardet–Biedl syndrome, nephronophthisis, and polycystic kidney disease. More recently, his group has expanded its research to investigate how primary cilia regulate stem cell differentiation, DNA damage responses, cellular senescence, and aging-associated cancers and neurodegenerative diseases, bridging fundamental cilia biology with disease mechanisms and therapeutic target discovery.

Dr. Hu’s research has been continuously supported by the National Institutes of Health (NIH), Department of Defense (DoD), American Society of Nephrology (ASN), and PKD Foundation. He has also served extensively on NIH and DoD grant review panels, including as Chair and standing member. His work has been published in leading journals, including Nature Cell Biology, Nature Genetics, Nature Communications, Science Translational Medicine, Science Advances, PNAS, Journal of Cell Biology, Kidney International, and Journal of the American Society of Nephrology. His research has had a significant impact on the fields of cilia biology, ciliary signaling, and the molecular pathogenesis of human ciliopathies.

Cellular senescence, characterized by persistent growth arrest and a pro-inflammatory senescence-associated secretory phenotype (SASP), is a hallmark of aging and a major contributor to age-related disease and tumorigenesis. However, the upstream mechanisms that initiate senescence remain poorly understood. Primary cilia are microtubule-based sensory organelles present on most mammalian cells. Ciliary dysfunction causes a wide spectrum of ciliopathies affecting virtually every major human organ system, yet how primary cilia communicate with intracellular stress-response pathways remains elusive. Here, we uncover a previously unrecognized cilium-to-nucleus pathway that triggers cellular senescence in response to persistent or irreparable stress. The ciliary protein FBF1 translocates from primary cilia to promyelocytic leukemia nuclear bodies (PML-NBs), nuclear hubs that coordinate stress responses and senescence, where it promotes PML-NB expansion and senescence initiation. Disrupting this pathway blocks senescence induction in primary human fibroblasts. Importantly, Fbf1-deficient mice exhibit reduced lifelong senescence burden, improved healthspan, and extended lifespan. Together, our findings reveal an unexpected cilium-nucleus signaling nexus that links cellular stress to senescence and establishes primary cilia as active regulators of mammalian aging and longevity.

All are welcome.