Schumacher Laboratory

About the Lab

The genome contains all information for building and functionally maintaining the cell. In contrast to any other macromolecule the genome cannot be replaced but instead requires constant repair amid tens of thousands of DNA damaging events that occur daily in a human cell. The consequences of DNA damage range from genetic aberrations such as mutations that can alter gene function to persistent lesions that can interfere with transcription and replication that can functionally impair the cell. Given the central role that the genome has for any biological process, the DNA damage response is a multi-factorial process that impinges on a plethora of homeostatic mechanisms.The Schumacher-Lab aims to understand the DNA repair and DNA damage response mechanisms in the context of living organisms.

In humans, DNA repair deficiencies can give rise to developmental defects, premature ageing, and cancer susceptibility. The pathologies observed in those congenital syndromes are highly complex. Therefore, we developed the nematode C. elegans as experimental model to shed light on the highly conserved DNA repair mechanisms and the consequences of DNA damage on the organism. C. elegans is particularly relevant for investigating the mechanisms of genome maintenance in germ cells that perpetuate the genetic information indefinitely throughout the generations. In contrast, the somatic tissues of the worm allow the identification of genome stability mechanisms in terminally differentiated cell types, such as neurons, that cannot be replaced but instead require lifelong maintenance and repair. Here, we are addressing who homeostatic mechanisms could maintain somatic functioning amid the onslaught of DNA damage throughout a lifespan. The germline and the soma are intricately communicating and influence each other’s maintenance mechanisms.

We are studying how impaired genome stability influences reproductive lifespan via stress response mechanisms in the soma and, vice versa, how the soma surveils the environment and regulates the genome quality control in the germ cells. Given the highly conserved DNA damage responses in the nematode we are using mammalian disease models and human cell culture to address their functional involvement in genome stability control in disease mechanisms. We are employing a wide variety of state-of-the-art approaches ranging from genetics and epigenetics, cell biology and biochemistry to transcriptomics and proteomics. In our lab, graduate and post-graduate biology, biochemistry, bioinformatics, and medical students work together with postdoc from diverse backgrounds to address the pertinent questions of the biology of ageing and age-related diseases.

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Lab PI Björn Schumacher

Since 2013, Björn Schumacher is full professor and director of the Institute for Genome Stability in Aging and Diseases (IGSAD) at the CECAD Research Centre of the University of Cologne. He received his PhD at the Max Planck Institute for Biochemistry in Munich and conducted his postdoctoral research as EMBO and Marie Curie fellow at the Erasmus Medical Centre in Rotterdam. Professor Schumacher is President of the German Society for DNA Repair (DGDR), co-Director of the Minerva Center of the Biological Mechanisms of Healthy Aging at Bar-Ilan University (IL), and between 2014 and 2020 served as President of the German Society for Aging Research (DGfA). Since 2023, Schumacher is speaker of the DFG Research Unit FOR 5504 on “Physiological causes and consequences of genome instability” and, since 2025, holds the ERA Chair in the Research and Innovation Program of Excellence on Aging and Longevity at the University of Crete, Greece. He was awarded with the Eva Luise Köhler Research Prize, the Innovation Prize of the State of North Rhine-Westphalia, the DFG Reinhart Koselleck and European Research Council (ERC) grants, coordinated the Marie Curie initial training network on chronic DNA damage in aging (CodeAge) and served on several editorial boards.

His research interest focuses on the molecular mechanisms through which DNA damage contributes to cancer development and aging-associated diseases. Employing the C. elegans system and mammalian disease models, his group uncovered cell-autonomous and systemic responses through which the organism adapts to accumulating DNA damage with aging. Through the understanding of the basic mechanisms of genome instability-driven aging, Schumacher aims to contribute to the development of future strategies to prevent aging-associated diseases.