In our lab, we study the regulation and molecular mechanism of nucleotide excision repair (NER). NER is a versatile DNA repair pathway that recognizes lesions that distort the DNA helix. NER can be initiated by damage detection throughout the genome, i.e. global genome NER, or by stalling of RNA polymerase II on a lesion, i.e. transcription coupled NER.

We study the molecular mechanism of NER (see Figure 1) by means of imaging, cell biology, genetics and proteomics. For our studies, we use both mammalian cells as well as the model organism C. elegans. We aim to understand how NER functions within chromatin, how the activity of each protein is regulate and how the activity of NER is organized in different cell types in vivo. Also, we study how NER dysfunction causes disease, such as xeroderma pigmentosum and Cockayne syndrome, and how NER protects cancer cells against chemotherapeutic drugs.

For more detailed information on the mechanism of NER and its relation to cancer and aging, you can read our elaborate review.