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Nucleic Acids Research Advance Access published online on September 16, 2009
Nucleic Acids Research, doi:10.1093/nar/gkp741
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© The Author(s) 2009. Published by Oxford University Press.
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.5/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Genome Integrity, Repair and Replication

Involvement of p54(nrb), a PSF partner protein, in DNA double-strand break repair and radioresistance

Shuyi Li1,2, Wendy W. Kuhne1, Anita Kulharya3, Farlyn Z. Hudson1, Kyungsoo Ha1, Zhen Cao1,4 and William S. Dynan1,2,3,5,*

1Institute of Molecular Medicine and Genetics, 2Department of Medicine, 3Department of Pathology, Medical College of Georgia, Augusta, Georgia, USA 4Department of Oncology, Wuhan University School of Medicine, Wuhan 430071, China and 5Cancer Center, Medical College of Georgia, Augusta, Georgia USA

*To whom correspondence should be addressed. Tel: +1 706 721 8753; Fax: +1 706 434 6440; Email: wdynan{at}mcg.edu

Received July 22, 2009. Revised August 20, 2009. Accepted August 23, 2009.

Mammalian cells repair DNA double-strand breaks (DSBs) via efficient pathways of direct, nonhomologous DNA end joining (NHEJ) and homologous recombination (HR). Prior work has identified a complex of two polypeptides, PSF and p54(nrb), as a stimulatory factor in a reconstituted in vitro NHEJ system. PSF also stimulates early steps of HR in vitro. PSF and p54(nrb) are RNA recognition motif-containing proteins with well-established functions in RNA processing and transport, and their apparent involvement in DSB repair was unexpected. Here we investigate the requirement for p54(nrb) in DSB repair in vivo. Cells treated with siRNA to attenuate p54(nrb) expression exhibited a delay in DSB repair in a {gamma}-H2AX focus assay. Stable knockdown cell lines derived by p54(nrb) miRNA transfection showed a significant increase in ionizing radiation-induced chromosomal aberrations. They also showed increased radiosensitivity in a clonogenic survival assay. Together, results indicate that p54(nrb) contributes to rapid and accurate repair of DSBs in vivo in human cells and that the PSF·p54(nrb) complex may thus be a potential target for radiosensitizer development.


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