Jurgen Marteijn started his career as a PhD student in the Central Hematology Laboratory at the Radboud University Medical Center, Nijmegen where he studied the role of the ubiquitin proteasome pathway during haematopoiesis. In 2006 he became a postdoc in the department of Genetics, were he subsequently started his independent research line to study the role of the post-translation modification ubiquitin during DNA-repair and DNA damage-associated signaling (Marteijn, JCB,2009 and van Cuijk, Nat.Com,2015). Using a quantitative proteomics approach to identify DNA damage induced ubiquitylation events, his research group identified UVSSA. This novel identified Transcription-Coupled Repair factor (TCR) is mutated in the UV-sensitive syndrome (Schwertman, Nat.Gen, 2012).
This finding enabled his lab to further dissect the regulation and molecular mechanism of TCR and to understand the severe clinical consequences associated with inherited TCR-defects. Using a combination of live-cell imaging and quantitative proteomics, his research group showed that chromatin remodeling is an essential process during the restart of transcription upon removal of transcription blocking lesions by TCR (Dinant, Mol.Cel, 2013). Furhtermore, his team revealed that the spliceosome is a key target of the DDR and defines a R-loop-dependent, non-canonical ATM activation by transcription-blocking lesions as an important event in the DNA damage response upon transcriptional stress (Tresini, Nature,2015).
- 2014: VIDI Grant of Netherlands Organisation for Scientific Research
- 2011: Erasmus MC Fellowship
- 2008: Veni Grant of Netherlands Organisation for Scientific Research
- Dinant, C., Ampatziadis-Michailidis, G., Lans, H., Tresini, M., Lagarou, A., Grosbart, M., ... & Fousteri, M. (2013). Enhanced chromatin dynamics by FACT promotes transcriptional restart after UV-induced DNA damage. Molecular cell, 51(4), 469-479.
- Schwertman, P., Lagarou, A., Dekkers, D. H., Raams, A., van der Hoek, A. C., Laffeber, C., ... & Marteijn, J. A. (2012). UV-sensitive syndrome protein UVSSA recruits USP7 to regulate transcription-coupled repair. Nature genetics, 44(5), 598.
- Tresini, M., Warmerdam, D. O., Kolovos, P., Snijder, L., Vrouwe, M. G., Demmers, J. A., ... & Mullenders, L. H. (2015). The core spliceosome as target and effector of non-canonical ATM signalling. Nature, 523(7558), 53.
- Van Cuijk, L., Van Belle, G. J., Turkyilmaz, Y., Poulsen, S. L., Janssens, R. C., Theil, A. F., ... & Vermeulen, W. (2015). SUMO and ubiquitin-dependent XPC exchange drives nucleotide excision repair. Nature communications, 6, 7499.
- Wienholz, F., Vermeulen, W., & Marteijn, J. A. (2017). Amplification of unscheduled DNA synthesis signal enables fluorescence-based single cell quantification of transcription-coupled nucleotide excision repair. Nucleic acids research, 45(9), e68-e68.