Although we use numerous model systems, yeast, human and mouse cells and mice, our aim remains unchanged: revealing new molecular mechanisms supporting adaptive regulation of chromatin, epigenetics and transcription in physiological and disease states. Our efforts concentrate on a new player in the field of chromatin and transcriptional regulation: SUMOylation. This post-translational modification is essential during development, stress response, and maintenance of cellular identity. Furthermore, it supports cancer, therefore SUMOylation inhibition is a promising inroad into new treatments. Nevertheless, the molecular mechanisms regulated by SUMOylation at the chromatin are unclear and characterizing them will be our objective in the following decades.

The recent discovery of an epigenetic obesogenic memory and epigenetic cancer fate in absence of DNA mutation emphasize the importance of understanding mechanisms that maintain epigenetic fate during cellular reprogramming and prevent diseases. To do so, we use state of the art high-throughput methods (ChIP-seq, ATAC-seq, CAGE, RIME, MS, Confocal microscopy, HiC, etc.), bioinformatics and classical biochemistry to identify the dynamics of chromatin structure and chromatin-bound factors’ sumoylation during adipocyte differentiation in human adipose stem cells and mouse models.

Our goal is to reveal the SUMO-dependent mechanisms safeguarding epigenetic fate to prevent development of obesity and cancer.

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