CV Science

Céline Morey PhD, Molecular and Cell Biology

Course and current status

1999-2004     Doctoral studies on mouse X-chromosome inactivation. Mouse Molecular Genetics Unit (Avner’s laboratory), Pasteur Institute, Paris.

2004     Ph.D in Cellular and Molecular Biology, Paris 5 University, Paris.

2004-2007 Post-doctoral studies on nuclear reorganisation of HoxB and HoxD clusters during ES cell differentiation and mouse development. W. Bickmore’s laboratory, Chromosome and Gene Expression Section, MRC-Human Genetics Unit, Edinburgh, UK. 

Since 2008 Staff scientist (CRCN with the INSERM)

Research topic 2008-2014: Interplay between gene expression, chromatin structure and nuclear organisation during X-chromosome inactivation in mouse pre-implantation embryos;  Mouse Molecular Genetics Unit, Pasteur Institute, Paris.

Research topic since 2014: Non-coding genes and their role in the regulation of X-chromosome inactivation during development, evolution and in pathological contexts; UMR7216 Epigenetics and Cell Fate, Université de Paris.

Scientific summary

Although the sequence of the entire human genome is now available, we are still far from understanding how this code is read and executed during embryo development to give rise to the adult organism. The current view is that cell lineage commitment is not only ensured by activation and repression of key transcription factors but also by epigenetic processes and by the non-coding genome.

To understand the relationship between these regulatory modes, we use X-chromosome inactivation as a paradigm. This epigenetic process leads to the stable silencing of one of the two X-chromosomes in female mammals and thereby, allows to re-equilibrate the dosage of X-linked products with males. X-inactivation is an essential mechanism tightly linked to cell differentiation and controlled by many non-coding players. This model allows us to question the function and mode of action of the non-coding genome in 1) the loss of pluripotency, 2) the stability of epigenetic processes and 3) the emergence of pathological contexts such as cancer. While X-inactivation occurs in all female mammals, the modalities diverge significantly between species, which also permits to address the contribution of non-coding players to the diversification of epigenetic processes during evolution. We address these questions using the cellular models of mouse and primate embryonic stem cells, directed differentiation protocols and during normal and pathological haematopoiesis.