Table of Contents Author Guidelines Submit a Manuscript
Journal of Nucleic Acids
Volume 2010 (2010), Article ID 319754, 8 pages
http://dx.doi.org/10.4061/2010/319754
Research Article

BLM Deficiency Is Not Associated with Sensitivity to Hydroxyurea-Induced Replication Stress

1Institut Curie, Centre de Recherche, Centre Universitaire, Bât. 110, 91405 Orsay, France
2CNRS, UMR 3348, 91405 Orsay, France

Received 11 May 2010; Accepted 19 July 2010

Academic Editor: Ashis Basu

Copyright © 2010 Kenza Lahkim Bennani-Belhaj et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Linked References

  1. N. A. Ellis, J. Groden, T.-Z. Ye et al., “The Bloom's syndrome gene product is homologous to RecQ helicases,” Cell, vol. 83, no. 4, pp. 655–666, 1995. View at Google Scholar · View at Scopus
  2. M. Otsuki, M. Seki, E. Inoue et al., “Functional interactions between BLM and XRCC3 in the cell,” Journal of Cell Biology, vol. 179, no. 1, pp. 53–63, 2007. View at Publisher · View at Google Scholar · View at Scopus
  3. E. Sonoda, M. S. Sasaki, C. Morrison, Y. Yamaguchi-Iwai, M. Takata, and S. Takeda, “Sister chromatid exchanges are mediated by homologous recombination in vertebrate cells,” Molecular and Cellular Biology, vol. 19, no. 7, pp. 5166–5169, 1999. View at Google Scholar · View at Scopus
  4. K. L. Bennani-Belhaj, S. Rouzeau, G. Buhagiar-Labarchède et al., “The Bloom syndrome protein limits the lethality associated with RAD51 deficiency,” Molecular Cancer Research, vol. 8, no. 3, pp. 385–394, 2010. View at Publisher · View at Google Scholar · View at Scopus
  5. R. Hand and J. German, “A retarded rate of DNA chain growth in Bloom's syndrome,” Proceedings of the National Academy of Sciences of the United States of America, vol. 72, no. 2, pp. 758–762, 1975. View at Google Scholar · View at Scopus
  6. F. Giannelli, P. F. Benson, S. A. Pawsey, and P. E. Polani, “Ultraviolet light sensitivity and delayed DNA chain maturation in Bloom's syndrome fibroblasts,” Nature, vol. 265, no. 5593, pp. 466–469, 1977. View at Google Scholar · View at Scopus
  7. U. Lonn, S. Lonn, U. Nylen, G. Winblad, and J. German, “An abnormal profile of DNA replication intermediates in Bloom's syndrome,” Cancer Research, vol. 50, no. 11, pp. 3141–3145, 1990. View at Google Scholar · View at Scopus
  8. S. L. Davies, P. S. North, and I. D. Hickson, “Role for BLM in replication-fork restart and suppression of origin firing after replicative stress,” Nature Structural and Molecular Biology, vol. 14, no. 7, pp. 677–679, 2007. View at Publisher · View at Google Scholar · View at Scopus
  9. V. A. Rao, C. Conti, J. Guirouilh-Barbat et al., “Endogenous γ-H2AX-ATM-Chk2 checkpoint activation in Bloom's syndrome helicase-deficient cells is related to DNA replication arrested forks,” Molecular Cancer Research, vol. 5, no. 7, pp. 713–724, 2007. View at Publisher · View at Google Scholar · View at Scopus
  10. J. German, “Bloom's syndrome,” Dermatologic Clinics, vol. 13, no. 1, pp. 7–18, 1995. View at Google Scholar · View at Scopus
  11. L. Wu, S. L. Davies, N. C. Levitt, and I. D. Hickson, “Potential role for the BLM helicase in recombinational repair via a conserved interaction with RAD51,” The Journal of Biological Chemistry, vol. 276, no. 22, pp. 19375–19381, 2001. View at Publisher · View at Google Scholar · View at Scopus
  12. V. Tripathi, T. Nagarjuna, and S. Sengupta, “BLM helicase-dependent and -independent roles of 53BP1 during replication stress-mediated homologous recombination,” Journal of Cell Biology, vol. 178, no. 1, pp. 9–14, 2007. View at Publisher · View at Google Scholar · View at Scopus
  13. S. Sengupta, A. I. Robles, S. P. Linke et al., “Functional interaction between BLM helicase and 53BP1 in a Chk1-mediated pathway during S-phase arrest,” Journal of Cell Biology, vol. 166, no. 6, pp. 801–813, 2004. View at Publisher · View at Google Scholar · View at Scopus
  14. O. Bischof, S.-H. Kim, J. Irving, S. Beresten, N. A. Ellis, and J. Campisi, “Regulation and localization of the Bloom syndrome protein in response to DNA damage,” Journal of Cell Biology, vol. 153, no. 2, pp. 367–380, 2001. View at Publisher · View at Google Scholar · View at Scopus
  15. S. Sengupta, S. P. Linke, R. Pedeux et al., “BLM helicase-dependent transport of p53 to sites of stalled DNA replication forks modulates homologous recombination,” EMBO Journal, vol. 22, no. 5, pp. 1210–1222, 2003. View at Publisher · View at Google Scholar · View at Scopus
  16. V. Tripathi, S. Kaur, and S. Sengupta, “Phosphorylation-dependent interactions of BLM and 53BP1 are required for their anti-recombinogenic roles during homologous recombination,” Carcinogenesis, vol. 29, no. 1, pp. 52–61, 2008. View at Publisher · View at Google Scholar · View at Scopus
  17. K. J. Ouyang, L. L. Woo, J. Zhu, D. Huo, M. J. Matunis, and N. A. Ellis, “SUMO modification regulates BLM and RAD51 interaction at damaged replication forks,” PLoS Biology, vol. 7, no. 12, Article ID e1000252, 2009. View at Publisher · View at Google Scholar · View at Scopus
  18. J. K. Karow, A. Constantinou, J.-L. Li, S. C. West, and I. D. Hickson, “The Bloom's syndrome gene product promotes branch migration of Holliday junctions,” Proceedings of the National Academy of Sciences of the United States of America, vol. 97, no. 12, pp. 6504–6508, 2000. View at Publisher · View at Google Scholar · View at Scopus
  19. A. J. van Brabant, T. Ye, M. Sanz, J. L. German III, N. A. Ellis, and W. K. Holloman, “Binding and melting of D-loops by the Bloom syndrome helicase,” Biochemistry, vol. 39, no. 47, pp. 14617–14625, 2000. View at Publisher · View at Google Scholar · View at Scopus
  20. C. Z. Bachrati, R. H. Borts, and I. D. Hickson, “Mobile D-loops are a preferred substrate for the Bloom's syndrome helicase,” Nucleic Acids Research, vol. 34, no. 8, pp. 2269–2279, 2006. View at Publisher · View at Google Scholar · View at Scopus
  21. S. Raynard, W. Bussen, and P. Sung, “A double holliday junction dissolvasome comprising BLM, topoisomerase IIIα, and BLAP75,” The Journal of Biological Chemistry, vol. 281, no. 20, pp. 13861–13864, 2006. View at Publisher · View at Google Scholar · View at Scopus
  22. L. Wu, C. Z. Bachrati, J. Ou et al., “BLAP75/RMI1 promotes the BLM-dependent dissolution of homologous recombination intermediates,” Proceedings of the National Academy of Sciences of the United States of America, vol. 103, no. 11, pp. 4068–4073, 2006. View at Publisher · View at Google Scholar · View at Scopus
  23. A. Machwe, L. Xiao, J. Groden, and D. K. Orren, “The Werner and Bloom syndrome proteins catalyze regression of a model replication fork,” Biochemistry, vol. 45, no. 47, pp. 13939–13946, 2006. View at Publisher · View at Google Scholar · View at Scopus
  24. C. Ralf, I. D. Hickson, and L. Wu, “The Bloom's syndrome helicase can promote the regression of a model replication fork,” The Journal of Biological Chemistry, vol. 281, no. 32, pp. 22839–22846, 2006. View at Publisher · View at Google Scholar · View at Scopus
  25. D. V. Bugreev, X. Yu, E. H. Egelman, and A. V. Mazin, “Novel pro- and anti-recombination activities of the Bloom's syndrome helicase,” Genes and Development, vol. 21, no. 23, pp. 3085–3094, 2007. View at Publisher · View at Google Scholar · View at Scopus
  26. M. Amor-Guéret, “Bloom syndrome, genomic instability and cancer: the SOS-like hypothesis,” Cancer Letters, vol. 236, no. 1, pp. 1–12, 2006. View at Publisher · View at Google Scholar · View at Scopus
  27. L. Wu, “Role of the BLM helicase in replication fork management,” DNA Repair, vol. 6, no. 7, pp. 936–944, 2007. View at Publisher · View at Google Scholar · View at Scopus
  28. G. M. Alvino, D. Collingwood, J. M. Murphy, J. Delrow, B. J. Brewer, and M. K. Raghuraman, “Replication in hydroxyurea: it's a matter of time,” Molecular and Cellular Biology, vol. 27, no. 18, pp. 6396–6406, 2007. View at Publisher · View at Google Scholar · View at Scopus
  29. O. Imamura, K. Fujita, A. Shimamoto et al., “Bloom helicase is involved in DNA surveillance in early s phase in vertebrate cells,” Oncogene, vol. 20, no. 10, pp. 1143–1151, 2001. View at Publisher · View at Google Scholar · View at Scopus
  30. M. Ababou, V. Dumaire, Y. Lécluse, and M. Amor-Guéret, “Cleavage of BLM and sensitivity of Bloom's syndrome cells to hydroxurea and UV-C radiation,” Cell Cycle, vol. 1, no. 4, pp. 262–266, 2002. View at Google Scholar · View at Scopus
  31. S. L. Davies, P. S. North, A. Dart, N. D. Lakin, and I. D. Hickson, “Phosphorylation of the Bloom's syndrome helicase and its role in recovery from S-phase arrest,” Molecular and Cellular Biology, vol. 24, no. 3, pp. 1279–1291, 2004. View at Publisher · View at Google Scholar · View at Scopus
  32. S. Dutertre, M. Ababou, R. Onclercq et al., “Cell cycle regulation of the endogenous wild type Bloom's syndrome DNA helicase,” Oncogene, vol. 19, no. 23, pp. 2731–2738, 2000. View at Google Scholar · View at Scopus
  33. S. Eladad, T.-Z. Ye, P. Hu et al., “Intra-nuclear trafficking of the BLM helicase to DNA damage-induced foci is regulated by SUMO modification,” Human Molecular Genetics, vol. 14, no. 10, pp. 1351–1365, 2005. View at Publisher · View at Google Scholar · View at Scopus
  34. M. Ababou, V. Dumaire, Y. Lécluse, and M. Amor-Guéret, “Bloom's syndrome protein response to ultraviolet-C radiation and hydroxyurea-mediated DNA synthesis inhibition,” Oncogene, vol. 21, no. 13, pp. 2079–2088, 2002. View at Publisher · View at Google Scholar · View at Scopus
  35. Y. Saintigny, F. Delacôte, G. Varès et al., “Characterization of homologous recombination induced by replication inhibition in mammalian cells,” EMBO Journal, vol. 20, no. 14, pp. 3861–3870, 2001. View at Publisher · View at Google Scholar · View at Scopus
  36. H. Zhao and H. Piwnica-Worms, “ATR-mediated checkpoint pathways regulate phosphorylation and activation of human Chk1,” Molecular and Cellular Biology, vol. 21, no. 13, pp. 4129–4139, 2001. View at Publisher · View at Google Scholar · View at Scopus
  37. G. Speit and P. Schütz, “The effect of inhibited replication on DNA migration in the comet assay in relation to cytotoxicity and clastogenicity,” Mutation Research, vol. 655, no. 1-2, pp. 22–27, 2008. View at Google Scholar · View at Scopus
  38. A. Matsuoka, C. Lundin, F. Johansson et al., “Correlation of sister chromatid exchange formation through homologous recombination with ribonucleotide reductase inhibition,” Mutation Research, vol. 547, no. 1-2, pp. 101–107, 2004. View at Publisher · View at Google Scholar · View at Scopus
  39. V. A. Rao, A. M. Fan, L. Meng et al., “Phosphorylation of BLM, dissociation from topoisomerase IIIα, and colocalization with γ-H2AX after topoisomerase I-induced replication damage,” Molecular and Cellular Biology, vol. 25, no. 20, pp. 8925–8937, 2005. View at Publisher · View at Google Scholar · View at Scopus
  40. Y.-H. Hsiang, M. G. Lihou, and L. F. Liu, “Arrest of replication forks by drug-stabilized topoisomerase I-DNA cleavable complexes as a mechanism of cell killing by camptothecin,” Cancer Research, vol. 49, no. 18, pp. 5077–5082, 1989. View at Google Scholar · View at Scopus
  41. J. Bartkova, Z. Hořejší, K. Koed et al., “DNA damage response as a candidate anti-cancer barrier in early human tumorigenesis,” Nature, vol. 434, no. 7035, pp. 864–870, 2005. View at Publisher · View at Google Scholar · View at Scopus
  42. V. G. Gorgoulis, L.-V. F. Vassiliou, P. Karakaidos et al., “Activation of the DNA damage checkpoint and genomic instability in human precancerous lesions,” Nature, vol. 434, no. 7035, pp. 907–913, 2005. View at Publisher · View at Google Scholar · View at Scopus