Jesper Svejstrup

Mechanisms of Transcription Laboratory

We study the interface between transcription and other DNA-related processes, such as DNA replication, recombination and repair. One of the hallmarks of human disease, including cancer, is de-regulation of gene expression: genes that are supposed to be silent become activated, and genes that need to be expressed become inactive.

Another characteristic of cancer cells is their unstable genomes; their inability to repair, or maintain the integrity of, DNA. It has also become clear that the act of expressing our genes (transcription) itself entails a significant risk for genome stability. However, the biochemical mechanisms that connect transcription and pathways maintaining genome integrity to ensure their safe co-existence are poorly studied.

We seek to understand gene expression and the maintenance of genome integrity, as well as the connection between these processes, using a combination of biochemical (including proteomics), genetic (including genomics) and cell biological techniques, primarily in human cells.

Selected publications

Williamson, L; Saponaro, M; Boeing, S; East, P; Mitter, R; Kantidakis, T; Kelly, GP; Lobley, A; Walker, J; Spencer-Dene, B; Howell, M; Stewart, A and Svejstrup, JQ (2017) UV irradiation induces a non-coding RNA that functionally opposes the protein encoded by the same gene. Cell 168, 843-855

Saponaro M, Kantidakis T, Mitter R, Kelly GP, Heron M, Williams H, Söding J, Stewart A, Svejstrup JQ.RECQL5 controls transcript elongation and suppresses genome instability associated with transcription stress. Cell. 2014;157(5):1037-49

Ehrensberger AH, Kelly GP, Svejstrup JQ. Mechanistic Interpretation of Promoter-Proximal Peaks and RNAPII Density Maps. Cell. 2013;154(4):713-5

Wilson MD, Harreman M, Taschner M, Reid J, Walker J, Erdjument-Bromage H, Tempst P, Svejstrup JQ. Proteasome-mediated processing of def1, a critical step in the cellular response to transcription stress. Cell. 2013;154(5):983-95.

Close P, East P, Dirac-Svejstrup AB, Hartmann H, Heron M, Maslen S, Chariot A, Söding J, Skehel M, Svejstrup JQ. DBIRD complex integrates alternative mRNA splicing with RNA polymerase II transcript elongation. Nature. 2012;484:386-9

Anindya R, Mari PO, Kristensen U, Kool H, Giglia-Mari G, Mullenders LH, Fousteri M, Vermeulen W, Egly JM, Svejstrup JQ. A ubiquitin-binding domain in Cockayne syndrome B required for transcription-coupled nucleotide excision repair. Mol Cell. 2010;38(5):637-48

Saeki H, Svejstrup JQ. Stability, Flexibility, and Dynamic Interactions of Colliding RNA Polymerase II Elongation Complexes. Molecular Cell. 2009;35:191-205

Somesh BP, Sigurdsson S, Saeki H, Erdjument-Bromage H, Tempst P, Svejstrup JQ. Communication between distant sites in RNA polymerase II through ubiquitylation factors and the polymerase CTD. Cell. 2007;129:57-68

Somesh BP, Reid J, Liu WF, Søgaard TM, Erdjument-Bromage H, Tempst P, Svejstrup JQ. Multiple Mechanisms Confining RNA Polymerase II Ubiquitylation to Polymerases Undergoing Transcriptional Arrest. Cell. 2005;121:913-23

Woudstra EC, Gilbert C, Fellows J, Jansen L, Brouwer J, Erdjument-Bromage H, Tempst P, Svejstrup JQ. A Rad26-Def1 Complex Co-ordinates Repair and RNA Polymerase II Proteolysis in Response to DNA Damage. Nature. 2002;415:929-933

An image of Jesper Svejstrup.

Jesper Svejstrup
+44 (0)20 379 62045

  • Qualifications and history
  • 1993 PhD, Aarhus University, Denmark
  • 1993 Postdoctoral Fellow, Stanford School of Medicine, USA
  • 1996 Established lab at the Imperial Cancer Research Fund, UK (in 2002 the Imperial Cancer Research Fund became Cancer Research UK)
  • 2011 Adjunct Professor, University of Copenhagen, Denmark
  • 2015 Group Leader, the Francis Crick Institute, London, UK