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Roopesh Anand

DNA Double-Strand Breaks & Genomic Instability

The integrity of the DNA in our cells is essential for normal cellular functions. However, DNA damage, caused by various endogenous and exogenous factors throughout life, can accumulate over time. While cells possess many intricate DNA repair mechanisms, their efficiency wanes with age, leading to the persistence of DNA lesions and genomic instability. This accumulation contributes to cellular senescence, a state of irreversible growth arrest, and drives the ageing process. Moreover, unrepaired DNA damage can result in mutations, compromising the fidelity of genetic information and exacerbating cellular dysfunction. As a consequence, tissues and organs experience functional decline, predisposing individuals to age-related diseases such as cancer, neurodegeneration and cardiovascular disorders. Both heritable and acquired defects in some DNA repair genes can result in accelerated ageing diseases that affect longevity. Understanding the nexus between DNA damage and ageing offers insights into the fundamental mechanisms underlying age-related changes and informs strategies to promote healthy ageing and longevity.

My laboratory is interested in elucidating the mechanisms of DNA double-strand break repair, one of the most toxic DNA lesions, and understanding how their dysfunction promotes ageing.

Positions held

  • Since 2024: Group Leader, Institute of Molecular Biology (IMB), Mainz
  • 2019 - 2024: Postdoctoral researcher, The Francis Crick Institute, London
  • 2016 - 2019: Postdoctoral researcher, Institute for Research in Biomedicine (IRB), Bellinzona


  • 2016: PhD in Tumor Biology, University of Zurich
  • 2011: MSc in Transfusion and Transplantation Sciences, University of Bristol
  • 2009: BSc in Medical laboratory Technology, Punjab Technical University 

Selected publications by Roopesh Anand

Fleury H, MacEachern MK, Stiefel CM, Anand R, Sempeck C, Nebenfuehr B, Maurer-Alcalá K, Ball K, Proctor B, Belan O, Taylor E, Ortega R, Dodd B, Weatherly L, Dansoko D, Leung JW, Boulton SJ and Arnoult N (2023) The APE2 nuclease is essential for DNA double-strand break repair by microhomology-mediated end joining. Mol Cell, 83:1429–1445 Link

Anand* R, Buechelmaier* E, Belan O, Newton M, Vancevska A, Kaczmarczyk A, Takaki T, Rueda DS, Powell SN and Boulton SJ (2022) HELQ is a dual-function DSB repair enzyme modulated by RPA and RAD51. Nature, 601:268–273 (*indicates equal contribution) Link

Belan O, Barros C, Kaczmarczyk A, Anand R, Federico S, O'Reilly N, Newton MD, Maeots E, Enchev RI, Martinez-Perez E, Rueda DS and Boulton SJ (2021) Single-molecule analysis reveals cooperative stimulation of Rad51 filament nucleation and growth by mediator proteins. Mol Cell, 81:1058–1073.e7 Link

Anand R, Jasrotia A, Bundschuh D, Howard SM, Ranjha L, Stucki M and Cejka P (2019) NBS1 promotes the endonuclease activity of the MRE11-RAD50 complex by sensing CtIP phosphorylation. EMBO J, 38:e101005 Link

Anand R, Ranjha L, Cannavo E and Cejka P (2016) Phosphorylated CtIP functions as a co-factor of the MRE11-RAD50-NBS1 endonuclease in DNA end resection. Mol Cell, 64:940–950 Link