In mammalian cells, all subunits of the DNA-dependent protein kinase (DNA- PK) have been implicated in the repair of DNA double-strand breaks and in V(D)J recombination. In the yeast, Saccharomyces cerevisiae, we have examined the phenotype conferred by a deletion of HDFI, the putative homologue of the 70-kD subunit of the DNA-end binding Ku complex of DNA-PK. The yeast gene does not play a role in radiation-induced cell cycle checkpoint arrest in G1 and G2 or in hydroxyurea-induced checkpoint arrest in S. In cells competent for homologous recombination, we could not detect any sensitivity to ionizing radiation or to methyl methanesulfonate (MMS) conferred by a hdfl deletion and indeed, the repair of DNA double-strand breaks was not impaired. However, if homologous recombination was disabled (rad52 mutant background), inactivation of HDFI results in additional sensitization toward ionizing radiation and MMS. These results give further support to the notion that, in contrast to higher eukaryotic cells, homologous recombination is the favored pathway of double-strand break repair in yeast whereas other competing mechanisms such as the suggested pathway of DNA-PK-dependent direct break rejoining are only of minor importance.
|Original language||English (US)|
|Number of pages||12|
|State||Published - Jan 1996|
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