Abstract
A human low-density-lipoprotein (LDL) receptor-deficient diploid fibroblast cell line (GM1915) was determined to be short patch competent (DNA polymerase-β) and long patch deficient (DNA polymerase-α) for DNA excision repair. Analysis of DNA from GM1915 cells or from WI38 control cells, following treatment with a mutagen known to initiate long patch excision repair, showed that GM1915 cells exhibited decreased resynthesis of oligonucleotide segments excised during repair. When cells deficient in DNA polymerase-α activity were permeabilized to permit LDL entry, repair synthesis immediately increased. These data suggest that DNA polymerase-α is not activated by mutagen treatment in GM1915 cells and that introduction of LDL into the cells results in activation of the enzyme.
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