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Molecular Biology and Genetics |
Department of Pathology, University of Washington, Seattle, Washington, 98195 [J. O., C. P.]; Life Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, California 94720 [S. H., J. C.]; and Department of Pathology, University of California at Los Angeles, Los Angeles, California 90095 [R. H. S.]
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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