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DNA double-strand breaks are not sufficient to initiate recruitment of TRF2

Nature Genetics volume 39, pages 696–698 (2007)Cite this article

To the Editor:

The human telomere binding factor TRF2 is essential at telomeres, facilitating the formation and stabilization of t-loops1 and suppressing local ATM-mediated damage response2. Bradshaw et al.3 recently reported that TRF2 accumulates at nuclear sites damaged by high-intensity laser beams, presumptively in response to DNA double-strand breaks (DSBs), and that it arrives before other DNA repair-related proteins, including ATM. To characterize the type of lesion responsible for triggering TRF2 recruitment, we produced a variety of localized nuclear damage and then quantified TRF2 colocalization with appropriate DNA damage markers. Although we found that TRF2 is indeed recruited to sites damaged by a high-intensity multiphoton laser beam, we did not find any evidence for such recruitment after we exposed cells to lower-intensity sources of ultraviolet radiation or to ionizing radiation, indicating that archetypal radiogenic DNA lesions such as DSBs are insufficient to trigger TRF2 recruitment.

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Figure 1: TRF2 response to photoinduced DNA damage.
Figure 2: TRF2 fails to colocalize with DNA damage generated by α-particle irradiation.

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Acknowledgements

We thank M. Cornforth for critical reading of the manuscript and for discussions. We also thank K. Mattern, D. van Gent and W. Vermeulen for providing cells; R.Y. Tsien for providing mCherry; C. Dinant for assistance with various laser-assisted local damaging techniques and C.H. van Oven and R.A. Hoebe for technical assistance. M.S.L. was supported by the Netherlands Organisation for Scientific Research (ZonMW 912-03-012). J.S., P.M.K. and J.A.A. were funded in part by a grant from the Dutch Cancer Society. E.S.W., R.L.U. and S.M.B. acknowledge support from the US National Institutes of Health (CA-09236 and CA-43322), US Department of Energy (DE-FG02-01ER63239) and the US National Aeronautics and Space Administration (NNJ04HD83G). The Radiological Research Accelerator Facility is supported through US National Institute of Biomedical Imaging and Bioengineering grant P41-EB002033.

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Author notes

  1. Eli S Williams and Jan Stap: These authors contributed equally to this work.

Authors and Affiliations

  1. Department of Environmental and Radiological Health Sciences, Cell and Molecular Biology Graduate Program, Colorado State University, Fort Collins, Colorado, USA

    Eli S Williams, Robert L Ullrich & Susan M Bailey

  2. Center for Microscopical Research (Department of Cell Biology and Histology), Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands

    Jan Stap, Przemek M Krawczyk & Jacob A Aten

  3. Department of Cell Biology and Genetics and Department of Radiation Oncology, Erasmus Medical Center, Rotterdam, The Netherlands

    Jeroen Essers

  4. Radiological Research Accelerator Facility, Center for Radiological Research, Columbia University, Irvington, New York, USA

    Brian Ponnaiya

  5. The Amsterdam Nuclear Organisation Group, Swammerdam Institute for Life Sciences, University of Amsterdam, Amsterdam, The Netherlands

    Martijn S Luijsterburg

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Supplementary information

Supplementary Fig. 1

Recruitment of repair proteins in response to laser microirradiation. (PDF 501 kb)

Supplementary Fig. 2

TRF2 recruitment to microirradiated regions in the absence of Hoechst. (PDF 161 kb)

Supplementary Fig. 3

Quantification of fluorescence intensity of TRF2 after longitudinal exposure to one or two α-particles. (PDF 75 kb)

Supplementary Fig. 4

Protein response to localized exposure of 400 α-particles. (PDF 229 kb)

Supplementary Table 1

Summary of protein responses after exposure to various DNA damaging sources. (PDF 76 kb)

Supplementary Methods (PDF 147 kb)

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Williams, E., Stap, J., Essers, J. et al. DNA double-strand breaks are not sufficient to initiate recruitment of TRF2. Nat Genet 39, 696–698 (2007). https://doi.org/10.1038/ng0607-696

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