Journal
EMBO REPORTS
Volume 6, Issue 6, Pages 551-556Publisher
WILEY
DOI: 10.1038/sj.embor.7400418
Keywords
DNA interstrand crosslinks; DNA repair; mismatch repair; psoralen
Categories
Funding
- NCI NIH HHS [R01 CA093729, P01 CA097175, CA97175, CA93729] Funding Source: Medline
- NIEHS NIH HHS [P30 ES007784, ES07784] Funding Source: Medline
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DNA interstrand crosslinks (ICLs) present formidable blocks to DNA metabolic processes and must be repaired for cell survival. ICLs are induced in DNA by intercalating compounds such as the widely used therapeutic agent psoralen. In bacteria, both nucleotide excision repair (NER) and homologous recombination are required for the repair of ICLs. The processing of ICLs in mammalian cells is not clearly understood. However, it is known that processing can occur by NER, which for psoralen ICLs can be an error-generating process conducive to mutagenesis. We show here that another repair pathway, mismatch repair (MMR), is also involved in eliminating psoralen ICLs in human cells. MMR deficiency renders cells hypersensitive to psoralen ICLs without diminishing their mutagenic potential, suggesting that MMR does not contribute to error-generating repair, and that MMR may represent a relatively error-free mechanism for processing these lesions in human cells. Thus, enhancement of MMR relative to NER may reduce the mutagenesis caused by DNA ICLs in humans.
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