Since 2010 : INSERM scientist at Laboratory of Biology and Modeling of the Cell (LBMC), Ecole Normale Supérieure de Lyon, Lyon (France)
2008 : HDR, Université de Lyon 1
2003-2010 : INSERM Scientist at Centre Léon Berard, Lyon, France. Eric Wattel's lab
2001-2002 : Post-doc at the Fusagx Gembloux (Belgium). Luc Willems' Lab
1997-2001 : PhD in Fondamental Virology, Université Paris 7 (France).
My research career is dedicated to investigating the molecular mechanisms that regulate leukemogenic processes during the infection by HTLV-1, the causative agent of adult T-cell leukemia/lymphoma (ATLL) and various inflammatory diseases. I initiated these investigations during my PhD under the supervision of Eric Wattel at the Institut de Recherche sur le Cancer de Lille (IRCL, France), where we made significant contributions to understanding HTLV-1 replication through clonal expansion and its association with cellular genomic instability. I furthered my research during my postdoctoral internship at FUSAgs Gembloux (Belgium), where I extended my investigations to the Bovine Leukemia Virus.
In 2002, I joined INSERM and established my own research group within the Centre Léon Bérard (CRCL) in Lyon, France, collaborating closely with E. Wattel. During this period, I focused on exploring the molecular mechanisms underlying viral persistence, particularly HTLV-1 and other deltaretroviruses like HTLV-II and BLV. Our studies provided insights into how these viruses manipulate cellular processes and reprogram gene expression, with a specific focus on the transcriptional changes associated with telomere maintenance.
In 2011, I transferred my research group to the Laboratory of Biology and Modeling of the Cell (LBMC) at ENS-Lyon. Here, we expanded our investigations to include post-transcriptional regulations induced by HTLV-1 infection, such as miRNA expression patterns and alternative splicing of coding and non-coding RNAs. Additionally, I collaborated with the Hospices Civils de Lyon on translational research, where we identified alternative splicing modifications as potential prognostic markers in acute myeloblastic leukemia.
Methodologically, we employed various approaches to address our research questions, including limited-dilution cloning of primary T-CD4+ cells, large-scale analysis of gene expression at the transcript and exon levels, miRNA quantification using chips and TLDA assays, mass spectrometry analysis of transcription factors through DNA affinity precipitation assays (DAPA), and more recently, the investigation of changes in 3D chromatin conformation using techniques like Hi-C, 3C, and 4C.
Currently, my research is dedicated to unraveling the molecular mechanisms that connect chromatin topology to alternative splicing decisions, specifically in the synthesis of linear and circular RNA isoforms during HTLV-1-associated leukemogenesis. These ongoing investigations aim to deepen our understanding of the complex interplay between chromatin organization and post-transcriptional regulations, with the ultimate goal of advancing our knowledge of HTLV-1-related pathologies.