This conference has many advantages for me: firstly, it gives me the opportunity to take an interest in fields other than my area of expertise, to talk to eminent people and to discover a working environment that is extremely different from my own. I enjoy exchanging ideas, sharing and learning. It's also a dream for me to be able to travel to Hong Kong and discover its culture and education, as well as the latest discoveries at the cutting edge of science. Finally, I've always enjoyed discussing my work and the way I imagine science. This forum will be the perfect opportunity to do both!

Pathogens co-evolve with their hosts, developing sophisticated strategies to evade immune defenses and manipulate host physiology. For example, Theileria annulata can transform and immortalize infected bovine leukocytes, inducing a cancer-like phenotype. Lacking a parasitophorous vacuole, this parasite likely uses unique mechanisms to hijack host signaling pathways. Although some secreted proteins like TaPin1 have been identified, these mechanisms remain poorly understood. This research project aimed to map and characterize Theileria’s secretome, assess its impact on the host epigenome, and clarify its role in maintaining the transformed phenotype. A pilot study identified two parasite proteins that translocate into the host nucleus. One of them, SPORF1, shows distinct nuclear localization. Proteomic analysis revealed interactions with key gene regulation complexes: CtBP and the non-canonical Polycomb repressive complex (ncPRC1.1.3). SPORF1 may relocalize these complexes, potentially altering gene expression by modifying the epigenetic mark H2K119Ub. Interestingly, SPORF1 resembles the viral oncoprotein E1A in its interaction profile and oncogenic potential.
Ongoing work using stable Theileria-infected cell lines expressing SPORF1-GFP explores its molecular effects on PRC1 complexes and gene expression. This could provide the first evidence that an Apicomplexan parasite can directly modify the host epigenome by hijacking PRC1.