This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Jiao, R.
Right arrow Articles by Stagljar, I.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Jiao, R.
Right arrow Articles by Stagljar, I.

 Previous Article  |  Next Article 

Molecular and Cellular Biology, June 2004, p. 4710-4719, Vol. 24, No. 11
0270-7306/04/$08.00+0     DOI: 10.1128/MCB.24.11.4710-4719.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Physical and Functional Interaction between the Bloom's Syndrome Gene Product and the Largest Subunit of Chromatin Assembly Factor 1

Renjie Jiao,1 Csanád Z. Bachrati,2 Graziella Pedrazzi,1 Patrick Kuster,1 Maja Petkovic,1 Ji-Liang Li,2 Dieter Egli,3 Ian D. Hickson,2 and Igor Stagljar1*

Institute of Veterinary Biochemistry and Molecular Biology,1 Institute of Molecular Biology, University of Zürich, CH-8057 Zürich, Switzerland,3 Cancer Research UK, Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, University of Oxford, Oxford OX3 9DS, United Kingdom2

Received 22 December 2003/ Returned for modification 20 January 2004/ Accepted 27 February 2004

Bloom's syndrome (BS) is a genomic instability disorder characterized by cancer susceptibility. The protein defective in BS, BLM, belongs to the RecQ family of DNA helicases. In this study, we found that BLM interacts with hp150, the largest subunit of chromatin assembly factor 1 (CAF-1), in vitro and in vivo. Colocalization of a proportion of the cellular complement of these two proteins is found at specific nuclear foci coinciding with sites of DNA synthesis in the S phase. This colocalization increases in the presence of agents that damage DNA or inhibit DNA replication. In support of a functional interaction between BLM and CAF-1, we show that BLM inhibits CAF-1-mediated chromatin assembly during DNA repair in vitro. Although CAF-1 activity is not altered in BLM-deficient cells, the absence of BLM does impair the ability of CAF-1 to be mobilized within the nucleus in response to hydroxyurea treatment. Our results provide the first link between BLM and chromatin assembly coupled to DNA repair and suggest that BLM and CAF-1 function in a coordinated way to promote survival in response to DNA damage and/or replication blockade.

* Corresponding author. Mailing address: Institute of Veterinary Biochemistry and Molecular Biology, University of Zürich, Winterthurstr. 190, CH-8057 Zürich, Switzerland. Phone: 41-1-635 54 74. Fax: 41-1-635 68 40. E-mail: stagljar{at}vetbio.unizh.ch.

Molecular and Cellular Biology, June 2004, p. 4710-4719, Vol. 24, No. 11
0022-538X/04/$08.00+0     DOI: 10.1128/MCB.24.11.4710-4719.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Selak, N., Bachrati, C. Z., Shevelev, I., Dietschy, T., van Loon, B., Jacob, A., Hubscher, U., Hoheisel, J. D., Hickson, I. D., Stagljar, I. (2008). The Bloom's syndrome helicase (BLM) interacts physically and functionally with p12, the smallest subunit of human DNA polymerase {delta}. Nucleic Acids Res 36: 5166-5179 [Abstract] [Full Text]  
  • Bethke, L., Webb, E., Murray, A., Schoemaker, M., Johansen, C., Christensen, H. C., Muir, K., McKinney, P., Hepworth, S., Dimitropoulou, P., Lophatananon, A., Feychting, M., Lonn, S., Ahlbom, A., Malmer, B., Henriksson, R., Auvinen, A., Kiuru, A., Salminen, T., Swerdlow, A., Houlston, R. (2008). Comprehensive analysis of the role of DNA repair gene polymorphisms on risk of glioma. Hum Mol Genet 17: 800-805 [Abstract] [Full Text]  
  • Brosh, R. M. Jr, Bohr, V. A. (2007). Human premature aging, DNA repair and RecQ helicases. Nucleic Acids Res 35: 7527-7544 [Abstract] [Full Text]  
  • Exner, V., Taranto, P., Schonrock, N., Gruissem, W., Hennig, L. (2006). Chromatin assembly factor CAF-1 is required for cellular differentiation during plant development. Development 133: 4163-4172 [Abstract] [Full Text]  
  • Schonrock, N., Exner, V., Probst, A., Gruissem, W., Hennig, L. (2006). Functional Genomic Analysis of CAF-1 Mutants in Arabidopsis thaliana. J. Biol. Chem. 281: 9560-9568 [Abstract] [Full Text]  
  • Kato, A., Inoue, H. (2006). Growth Defect and Mutator Phenotypes of RecQ-Deficient Neurospora crassa Mutants Separately Result From Homologous Recombination and Nonhomologous End Joining During Repair of DNA Double-Strand Breaks. Genetics 172: 113-125 [Abstract] [Full Text]  
  • Linger, J., Tyler, J. K. (2005). The Yeast Histone Chaperone Chromatin Assembly Factor 1 Protects Against Double-Strand DNA-Damaging Agents. Genetics 171: 1513-1522 [Abstract] [Full Text]  
  • Petkovic, M., Dietschy, T., Freire, R., Jiao, R., Stagljar, I. (2005). The human Rothmund-Thomson syndrome gene product, RECQL4, localizes to distinct nuclear foci that coincide with proteins involved in the maintenance of genome stability. J. Cell Sci. 118: 4261-4269 [Abstract] [Full Text]  


Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»