Maxim GreenbergChercheur CNRS à l'Institut Jacques Monod (CNRS/Université de Paris) dans l'équipe "Dynamique de la chromatine dans le développement des mammifères"
Mes recherches
Originally from the United States, I did my PhD at the University of California at Los Angeles (UCLA) in the laboratory of Steve Jacobsen, where I studied the mechanisms of DNA methylation in the model plant, Arabidopsis thaliana. I arrived in Paris in 2012 to do my post-doctoral fellowship in the laboratory of Deborah Bourc'his at the Institut Curie. There I continued my research in the field of DNA methylation, but in the context of mouse development. I was recruited by the CNRS as a Chargé de Recherche in 2017. After obtaining my ATIP-Avenir and an ERC starting grant in 2019, I joined the Institut Jacques Monod where I have set up an independent research program centered on mammalian epigenetics.
Mon projet ATIP-Avenir
DyNAmecs
Immediately after fertilization, mammalian genomes undergo a dramatic reshaping of the epigenome as the embryo transitions from the zygote into the pluripotent cells primed for lineage commitment. This is best exemplified by DNA methylation reprogramming, as the gametic patterns are largely erased, and the embryonic genome undergoes a wave of de novo DNA methylation. Moreover, once DNA methylation patterns are established, mechanisms faithfully maintain the mark across cell division.
For my proposed research I utilize both a cell-based system that recapitulates these early embryonic events as well as an in vivo mouse model to investigate the extent and mechanisms of non-canonical DNA methylation functions. I plan to use a combinatorial approach of genomics, genetics, and proteomics in order to ascertain novel insights into DNA methylation-based regulation. Furthermore, I plan to employ precision epigenome editing tools to address the locus-specific impact of DNA methylation. Ultimately, I strive to gain a clear understanding of the profound epigenetic consequences of DNA methylation on this window of development, which occurs in the first week of mouse embryogenesis, and the second of human, but the repercussions of which can ripple throughout life.