Stopping DNA Replication in Its Tracks

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Science  09 Jul 1999:
Vol. 285, Issue 5425, pp. 212-213
DOI: 10.1126/science.285.5425.212

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Xeroderma pigmentosum (XP) patients have a greatly increased susceptibility to sunlight-induced skin cancer. Although three-quarters of patients are known to have defects in the nucleotide-excision repair pathway that repairs UV-damaged DNA, the remainder have no apparent defects in this repair pathway. As James Cleaver explains in his Perspective, this mystery has now been solved with the finding ( Johnson et al.) that these patients lack Pol h, a DNA polymerase that does not make errors during replication and that is crucial for bypassing UV-induced DNA lesions (called photoproducts). In the absence of Pol h, a related polymerase, Pol z which is extremely prone to errors-replicates the damaged DNA, resulting in daughter strands that are riddled with mistakes.