Gene regulatory network of white / beige adipocyte conversion

Project leader:Nolwenn Briand (adipose biology), Philippe Collas (nuclear biology)
Info:Configuration of the genome and interactions of chromatin with the nuclear lamina are important regulators of differentiation of adipose progenitor cells into adipocytes. Mutations in A-type lamins cause familial partial lipodystrophy of Dunnigan type FPLD2 (among other laminopathies) and affect adipose tissue in a depot-specific manner, leading to metabolic diseases. Using patient-derived cells and engineered adipose progenitors, we investigate the mechanisms controlling white and thermogenic beige adipogenesis, and how lipodystrophic lamin A mutations deregulate adipose depot-specific progenitors.

Nolwenn Briand, Natalia Galigniana, Sarah Hazel Pickering, Anita Sørensen, Mohamed Abdelhalim, Thomas Sæther

Ongoing research

Chromatin-associated mechanisms of regulation of upper vs. lower body fat tissue expansion
Lamin-chromatin interactions and spatial genome organization during white and beige adipogenesis, and after white-to-beige adipocyte conversion

Recent findings

Constitutive and variable LADs during adipogenic differentiation (Rønningen 2015 Genome Res)
Dynamic interactions of lamin A/C with promoters during adipogenic differentiation (Lund 2013 Genome Res)