Philippe Arnaud Ph.D Molecular and Cellular Biology

Course and current status

2011-          PI/ CNRS Staff scientist-GReD  UMR CNRS 6293/INSERM1103          /Clermont Université; Clermont-Ferrand, France

                      PI of the team: “Genetic and epigenetic control of cell lineage commitment during mouse development”.

2004 - 2011    CNRS Staff scientist- IGMM UMR5535, Montpellier, France

                   Dr. Robert Feil’s Team

                  Topic: Role of histone modifications in genomic imprinting in mammals..


2000-2003      Post-Doctoral Position - Babraham Institute, Cambridge,

                        Dr. Gavin Kelsey’s Team

                      Topic: Mechanisms leading to germline specific acquisition of DNA                                 methylation imprints in mammals.


1996-2000      Ph.D  Training - Université Blaise Pascal, Clermont-Ferrand.

                           Pr. J-M. Deragon’s team

                    Topic: DNA methylation and Host defense hypothesis : The   plant    SINE  S1Bn as a model.

Scientific summary

Correct embryonic development of organisms relies on the unique capability of pluripotent stem cells to differentiate in (almost) all cell types of the organism. During this tightly regulated process stem cells progressively develop a narrower potential that ultimately results in commitment to a specific cell fate with specific gene expression profiles and functional properties. This developmental program requires the concerted action of sequence-specific transcription factors and cell signalling, but it is also accompanied or caused by epigenetic modifications such as DNA methylation and histone modifications.

To address if and how histone modifications could be part of a –short-term– flexible epigenetic silencing mechanism, potentially involved in cell fate decisions, we are focusing  on unusual structures that contain both active (H3K4me2/3) and repressive (H3K27me3) chromatin marks. These so-called bivalents domains offer thus a plastic chromatin organization that has been proposed to mark genes that are “poised” for expression to occur in response to appropriate developmental cues. By using genomic imprinting in mammals as a model we aim to dissect mechanisms controlling bivalent chromatin domains during germline epigenetic reprogramming and throughout lineage commitment.

Key words:

epigenetic regulation ; genomic imprinting ; bivalent chromatin; histone demethylase; mammalian cell culture and differentiation; mouse Primordial germ cells; tumorigenesis.

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