Mechanisms of ageing and senescence

Destabilization of the genome

Cellular senescence is considered to be caused by the accumulation of damaged molecules with age, by telomere shortening or oncogene activation. Within this broad field, the FLI research groups study:


  • Genome surveillance and stability
        (i) replication and cell cycle control: the role of helicases (WRN), topoisomerases and the cell cycle protein Cdc45 (Grosse, Herrlich)
        (ii) DNA damage and repair: ATM, ATR, NBS1 and PARP-1/PARG; genetic mutations predisposing for radiosensitivity in tumor patients (Greulich, Herrlich, Wang)
        (iii) chromosome segregation: the anaphase promoting complex/cyclosome (APC/C), BubR1 (Diekmann)
  • Structure, function and biomolecular interaction of enzymes involved in the repair of oxidative damage of proteins (Görlach)
  • Translocation of chromatin proteins into PML nuclear bodies, which is one of the earliest steps in the senescence program (Diekmann)
  • Age-dependent changes of DNA methylation of the human genome (Platzer)
  • Telomere biology, using our life span model Nothobranchius furzeri as well as comparative genomics of a novel telomere maintenance system in social amoeba (Platzer)


senescence Destabilization of the genome Longevity Support Senescence Diseases


Last update: March 20, 2008