CV Science

jerome jullien PhD Life Science

Course and current status

2022-present       Team Leader Cell and gene engineering in tolerance, fertility and regenerative medicine CR2TI-UMR1064, Nantes, France

2019-2021          Principal Investigator Team2 CRTI-UMR1064, Nantes, France

                          Developmental epigenetics

2012-2019          Senior research associate: Gurdon group, The Wellcome Trust Gurdon Institute, Cambridge, UK.

                          Epigenetic mechanisms stabilising cell fate

                          Programming of sperm for development

2007-2012          Postdoctoral researcher: Gurdon group, The Wellcome Trust Gurdon Institute, Cambridge, UK.

                          Oocytes specific reprogramming factors

2003-2007          Postdoctoral researcher: Gurdon group, The Wellcome Trust Gurdon Institute, Cambridge, UK.

                          Ligand/receptor trafficking during morphogen gradient formation and interpretation  

2001-2003          Research scientist: Aptanomics (Biotech company), Ecole Normale Supérieure de Lyon, France.

                          Isolation and characterization of peptide aptamers inhibiting Bax induced cell death.

1997-2001          PhD in cell biology, Differentiation and cell cycle group of Brian B. Rudkin, Molecular and Cellular Biology Laboratory, Ecole Normale Supérieure de Lyon, France:

                         Expression and fate of nerve growth factor (NGF) receptor TrkA and p75^NTR.

Scientific summary

J Jullien’s group investigates the epigenetic mechanisms responsible for the establishment and maintenance of cell fate:

• Epigenetic programming of sperm for the regulation of early embryonic development

At fertilisation the sperm deliver to the embryo paternal genomic information, as well as epigenetic information such as those encoded in DNA methylation, post translational modifications of histones, and small RNAs. We are interested in evaluating the contribution of these epigenetic cues in the normal development of embryos, in particular in the regulation of gene expression and the establishment of early embryonic cell fate. We also investigate how such sperm mediated epigenetic inheritance could be hijacked to transmit paternal experience of the environment to the next generation.

• Epigenetic reprogramming of cell fate

During development, cells acquire distinct cell fate that need to be stabilised in order to ensure organismal health. We want to identify the epigenetic mechanisms involved in the stabilisation of cell identity. To that end, we use somatic cell nuclear transfer to egg or oocyte to challenge the epigenetic mechanism responsible for the stabilisation of cell identity and resist the reprogramming of cell fate. By identifying these epigenetic mechanisms of resistance to change  we hope to improve reprogramming processes for therapeutical purposes as well as identify disruption in epigenetic mechanisms associated with ageing or diseases such as cancer.

• The role of the immune system in cell fate changes during regeneration

Regenerative properties vary greatly between organisms. Following amputation for example while amphibian can fully regenerate lost appendages, mammals are unable to do so. Following injury or loss, a complex sequence of cellular and molecular events is initiated to repair damage/replace lost tissue. Early in this process, components of the immune system are recruited and are thought to regulate multiple events underlying regeneration and repair. We aim to evaluate  the mechanisms by which immune cells can either favour or antagonize the regenerative process depending on context or species. By carrying out cross species analysis, we hope to identify actionable regulatory events in the immune reaction to potentiate regeneration & repair in non-regenerative species.