Nicolas Gilbert
  • E-mail :[email]
  • Phone : 04 67 33 94 88
  • Location : Montpellier, France
Last update 2021-09-27 12:45:32.942

Nicolas Gilbert Ph.D. Molecular Biology

Course and current status


1992-1993:        “Maîtrise” of Cellular Biology and Genetic, Université Pierre et Marie Curie (Paris 6), France.

1993-1994:        “Diplôme d’Étude Approfondie” (DEA) of Cellular and Molecular Biology, Université Blaise Pascal (Clermont-Ferrand 2), France. (Equivalent of the Master degree of Sciences)

1994-1999:        Ph.D. degree, Molecular Biology, Université de Montréal, Canada, and Université Blaise Pascal (Clermont-Ferrand 2), France. (Cotutelle)

2011 ;            HDR, Habilitation à Diriger les Recherches, Université Montpellier II, France

Professional experience

1999-2003:    Post-doctoral fellow in the laboratory of John V. Moran at the Human Genetics Dept., University of Michigan, USA. Research topics: Mobilization of transcribed sequences by the retrotransposition machinery from human L1 elements.

2004-2009:    Research associate (CR1) at Institut de Génétique Humaine, UPR1142, Montpellier, France. Research topics: Study of human LINE-1 retrotransposition.   

2010-2014:    Group leader at the Institut de Génétique Humaine, UPR 1142, Montpellier, France. Research topics: Mobile elements, integrity and plasticity of the human genome.

2015-2016:    Research associate at the IRMB, INSERM U1183, Montpellier, France, Research topics: Mobile elements, integrity and plasticity of the human genome.

2016-2018:    Visiting Scientist at Institut Pasteur of Shanghai, Chinese Academy of Sciences, China, in the group of L. Jiang. Research topics: Pathogen-host interaction and Epigenetics.

2018-:            Research associate at the IRMB, INSERM U1183, Montpellier, team “Genome and stem cell plasticity in development and ageing”.

Scientific summary

The LINE-1 (L1) retrotransposon is the most abundant mobile element in the human genome. Approximately 100 elements remain potentially active and can therefore induce genetic diseases by insertional mutation in coding or regulatory regions. Moreover, due to its high representation in the genome (17%), L1 can generate deleterious genomic rearrangements induced by various mechanisms.

For two decades now, I have been studying the molecular mechanisms of L1 transposition and its impact on the genome. More recently, we are developing bioinformatics tools and performing in silico analyses to reveal the involvement of L1 in cancer genomic variability.

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