DNA interstrand crosslink repair in mammalian cells
Version of Record online: 18 MAY 2009
Copyright © 2009 Wiley-Liss, Inc.
Journal of Cellular Physiology
Volume 220, Issue 3, pages 569–573, September 2009
How to Cite
McCabe, K. M., Olson, S. B. and Moses, R. E. (2009), DNA interstrand crosslink repair in mammalian cells. J. Cell. Physiol., 220: 569–573. doi: 10.1002/jcp.21811
- Issue online: 25 JUN 2009
- Version of Record online: 18 MAY 2009
- Manuscript Accepted: 2 APR 2009
- Manuscript Received: 31 MAR 2009
- NHLBI Program Project Grant. Grant Number: 1PO1HL48546
DNA damage by agents crosslinking the strands presents a formidable challenge to the cell to repair for survival and to repair accurately for maintenance of genetic information. It appears that repair of DNA crosslinks occurs in a path involving double strand breaks (DSBs) in the DNA. Mammalian cells have multiple systems involved in the repair response to such damage, including the Fanconi anemia pathway that appears to be directly involved, although the mechanisms and site of action remain elusive. A particular finding relating to deficiency of the Fanconi anemia pathway is the observation of chromosomal radial formations after ICL damage. The basis of formation of such chromosomal aberrations is unknown although they appear secondarily to DSBs. Here we review the processes involved in response to DNA interstrand crosslinks which might lead to radial formation and the role of the nucleotide excision repair gene, ERCC1, which is required for a normal response, not just to DNA crosslinks, but also for DSBs at collapsed replication forks caused by substrate depletion. J. Cell. Physiol. 220: 569–573, 2009. © 2009 Wiley-Liss, Inc.