About our research
In adipose tissue, populations of adipocyte progenitors give rise to lipid-storing white adipocytes and energy-dissipating (thermogenic) beige adipocytes. Gene expression programs that govern lineage-specific differentiation and cell identity are blueprinted by the 3-dimensional layout of the genome. We study how nuclear lamina-chromatin interactions, 3D enhancer connectivity, chromatin accessibility, and transcription factor binding and activity collectively regulate adipose stem cell fate, using in vitro adipocyte differentiation models.
Laminopathies are nuclear lamin-linked diseases that include muscle dystrophies, progeria and partial lipodystrophy of Dunnigan-type (FPLD2). Deficiencies in lipid storage capacity of adipocytes in FPLD2 patients limit fat tissue expandability and exposes other organs to lipotoxicity. We study how lamin A mutations causing FPLD2 affect the 3D genomic landscape of adipogenic gene expression programs.
Cancer metastasis, including EMT, involves nuclear lamins, in as yet unclear ways. We study how the interplay between lamins and transcription factors contribute to regulating EMT and metastasis.
We investigate how microproteins, coded by short open reading frames, regulate transcription and epigenetic control of gene expression using healthy and cancer cell systems, and murine models. We explore the fundamental molecular mechanisms governing transcription factor regulation and translate these insights into innovative applications.
We combine molecular biology, microscopy, functional genomics, and bioinformatics approaches using patient cells, adipose stem cells, in vitro EMT models, and cancer cell lines.
Current topics
25 years of our lab’s research...
- 3D transcriptional landscape of beige adipocytes (Hazell-Pickering 2026 Commun Biol)
- RNA splicing during white and beige adipocyte differentiation (Hazell Pickering 2024 Front. Endocrinol)
- LncRNA HOTAIR and adipocyte function (Potolitsyna 2022 Sci Reports; Potolitsyna 2022 BMC Genomics)
- Euchromatic active regions and enhancer connectivity in lamina-associated domains (LADs) during early adipogenesis (Madsen-Østerbye 2022 Genome Biol; Madsen-Østerbye 2023 Genes)
- 3D genome modeling with Chrom3D (Paulsen 2017 Genome Biol; Paulsen 2018 Nature Protoc): https://github.com/Chrom3D/Chrom3D and TAD cliques during adipose differentiation: (Paulsen 2019 Nature Genet; Liyakat Ali 2021 BMC Genomics)
- Laminopathy-causing lamin A mutation deregulates endothelial and adipogenic differentiation (Briand 2018 Hum Mol Genet; Oldenburg 2017 J Cell Biol; Oldenburg 2014 Hum Mol Genet)
- LADs during adipose differentiation (Lund 2013 Genome Res; Lund 2015 Nucl Acids Res; Rønningen 2015 Genome Res); EDD package for LAD detection: https://github.com/CollasLab/edd
- Deposition of histone variant H3.3 into chromatin (Delbarre 2010 Mol Biol Cell, 2013 Genome Res, 2017 Genome Res; Ivanauskiene 2014 Genome Res)
- Epigenetic patterning of developmental gene expression (Lindeman 2011 Dev Cell; Andersen 2012 Genome Biol) and adipocyte differentiation (Boquest 2007 Stem Cells; Sørensen 2010 Mol Biol Cell; Shah 2014 BMC Genomics; Rønningen 2015 Genome Res)
- Chromatin immunoprecipitation (ChIP) for small cell numbers (Dahl 2008 Nature Protoc; Dahl 2009 Genome Biol)
- Cell reprogramming (Håkelien 2002 Nature Biotech; Taranger 2005 Mol Biol Cell; Freberg 2007 Mol Biol Cell)
- Disassembly and reformation of the nuclear envelope (Steen 2000 J Cell Biol; Steen 2001 J Cell Biol; Martins 2003 J Cell Biol)
- And close to 50 alumni...
