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, 62 (2), 547-51

Lack of WRN Results in Extensive Deletion at Nonhomologous Joining Ends

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  • PMID: 11809708

Lack of WRN Results in Extensive Deletion at Nonhomologous Joining Ends

Junko Oshima et al. Cancer Res.

Abstract

Loss of WRN causes the genomic instability progeroid syndrome, Werner syndrome. WRN encodes a multifunctional nuclear protein with 3'-->5' exonuclease and 3'-->5' helicase activities. Linear plasmids with noncompatible ends introduced to Werner syndrome cells underwent extensive deletions at nonhomologous joining ends, particularly at the 3' protruding single-stranded end. This extensive deletion phenotype was complemented by wild-type WRN. These results suggest that WRN can out-compete other exonucleases that participate in double-strand break repair or stabilize the broken DNA end.

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