“DNA damage unifies the theories of ageing !?”
Prof. Björn Schumacher
In 2009, Dr. Björn Schumacher was appointed as an independent junior group leader in the CECAD Excellence Cluster for Ageing Research. He studied biology at the University of Constance, Germany, and the University of Stony Brook, NY. He received his PhD training at the Max Planck Institute for Biochemistry in Martinsried, Germany, after which he performed his post-doctoral research as an EMBO long-term and Marie Curie intra-European fellow at the Erasmus Medical Centre in Rotterdam, the Netherlands. In 2009, Schumacher was awarded with the Innovation prize for young researchers of the State of Northrhine-Westphalia and in 2010, he received the highly prestigious ERC starting independent researcher grant.
Björn Schumacher‘s goup investigates the fundamental mechanisms through which genome instability leads to ageing.
Previous scientific achievements
Using systems biology approaches, Dr. Björn Schumacher has revealed shared response pathways that are evoked in premature ageing and in extended longevity as well as identified mechanisms through which cells respond to increasingly damaged genomes with ageing. Moreover, the Schumacher group has established conserved DNA-repair mechanisms in the genetic model systems C. elegans that in human underlie cancer predisposition and premature ageing syndromes.
Within Sybacol, the Schumacher group has taken on the challenge to identify the complex regulatory networks that mediate responses to increasing loads of DNA damage that causally contribute to the functional deterioration of cells and tissue when they age. The Schumacher lab is studying rare congenital cancer predisposition and progeroid syndromes that are caused by mutations in DNA-repair factors. For this purpose, the group is employing comprehensive gene expression analyses that are instrumental in generating hypotheses concerning the underlying regulatory pathways. Thus, derived hypotheses will be evaluated by genetic and biochemical methodologies using the powerful genetics of C. elegans, a biological model system with fundamental importance in ageing research. Finally, the function of novel regulatory pathways will be evaluated in human progeroid syndromes and ageing-associated diseases.
Garinis, G.A., Uittenboogaard, L.M., Stachelscheid, H., Fousteri, M., van Ijcken, W., Breit, T.M., van Steeg, H., Mullenders, L.H., van der Horst, G.T., Bruning, J.C., Niessen, C.M., Hoeijmakers, J.H., and Schumacher, B.: Persistent transcription-blocking DNA lesions trigger somatic growth attenuation associated with longevity. Nat Cell Biol. (2009); 11(5): 604-615.
Schumacher, B., van der Pluijm, I., Moorhouse, M.J., Kosteas, T., Robinson, A.R., Suh, Y., Breit, T.M., van Steeg, H., Niedernhofer, L.J., van Ijcken, W., Bartke, A., Spindler, S.R., Hoeijmakers, J.H., van der Horst, G.T., and Garinis, G.A.: Delayed and accelerated aging share common longevity assurance mechanisms. PLoS Genet. (2008); 4(8): e1000161.
Schumacher, B., Garinis, G.A., and Hoeijmakers, J.H.: Age to survive: DNA damage and aging. Trends Genet. (2008); 24(2): 77-85.
Schumacher, B., Hanazawa, M., Lee, M.H., Nayak, S., Volkmann, K., Hofmann, E.R., Hengartner, M., Schedl, T., and Gartner, A.: Translational repression of
C. elegans p53 by GLD-1 regulates DNA damage-induced apoptosis. Cell. (2005); 120(3): 357-368.
Schumacher, B., Hofmann, K., Boulton, S., and Gartner, A.: The C. elegans homolog of the p53 tumor suppressor is required for DNA damage-induced apoptosis. Curr Biol. (2001); 11(21): 1722-1727.