Research Cell Systems & Imaging

Research focus

  • We specialise in cell-centered research, with particular focus on the role of the cell nucleus in accelerated aging diseases
  • Relying on a multidisciplinary cocktail of techniques incl. genome editing, advanced light microscopy and image informatics, we aim at generating insights in disease development
  • Our generic interest in gauging cellular health condition with quantitative microscopy directly connects to environmental monitoring applications, an approach we refer to as exposome screening.

Laminopathies are genetic diseases that target specific tissues such as adipose, muscle or nerves, but can also act systemically to induce progeria or metabolic syndromes. Despite the bewildering diversity of disease manifestations, all these pathologies share a common cellular feature: defects of the nuclear lamina, a filamentous network that delineates the cell nucleus. How these defects contribute to disease development is, however, not yet fully understood. With an eye on novel diagnostic and therapeutic strategies, we aim to enhance the fundamental understanding of laminopathies from a cell-centered perspective. We have recently discovered that lamin defects interfere with nucleocytoplasmic compartmentalization. We suspect this feature to contribute significantly to disease development. To bypass scarcity and heterogeneity of patient material, we are developing model cell lines that express pathology-causing mutations from the endogenous locus. In parallel, high-content and multimodal imaging strategies are being optimized on experimental models to enhance in cellula diagnostics.


montage

Key references

J. Robijns, F. Molenberghs, T. Sieprath, T. Corne, M. Verschuuren and W. De Vos (2016). In silico synchronization reveals regulators of nuclear ruptures in lamin A/C deficient model cells. Scientific reports 6(30325), p. 1-11.

T. Sieprath, T. Corne, M. Noteboom , C. Grootaert , A. Rajkovic , B. Buysschaert, J. Robijns, J. Broers, F. Ramaekers, W. Koopman, P. Willems and W. De Vos (2015). Sustained accumulation of prelamin A and depletion of lamin A/C both cause oxidative stress and mitochondrial dysfunction but induce different cell fates.Nucleus 6 (3), p. 236-246.

W. De Vos, F. Houben, M. Kamps, J. Cox, P. Van Oostveldt, V. Verstraeten, M. van Steensel, C. Marcelis, A. van den Wijngaard, F. Ramaekers and J. Broers (2011).Repetitive Disruptions of the Nuclear Envelope Invoke Temporary Loss of Cellular Compartmentalization in Laminopathies. Human Molecular Genetics 20(21), p.4175-4186.

W. De Vos, F. Houben, R. A. Hoebe, R. Hennekam, B. Van Engelen, E. Manders, F. Ramaekers, J. Broers and P. Van Oostveldt (2010). Increased plasticity of the nuclear envelope and hypermobility of telomeres due to the loss of A-type lamins. Biochimica et Biophysica Acta – General Subjects 1800(4), p.448-458.





Staffmembers