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- W1774053018 abstract "Abstract In this report, we investigated the phenotypes caused by temperature-sensitive (ts) mutant alleles of dna2+ of Schizosaccharomyces pombe, a homologue of DNA2 of budding yeast, in an attempt to further define its function in vivo with respect to lagging-strand synthesis during the S-phase of the cell cycle. At the restrictive temperature, dna2 (ts) cells arrested at late S-phase but were unaffected in bulk DNA synthesis. Moreover, they exhibited aberrant mitosis when combined with checkpoint mutations, in keeping with a role for Dna2 in Okazaki fragment maturation. Similarly, spores in which dna2+ was disrupted duplicated their DNA content during germination and also arrested at late S-phase. Inactivation of dna2+ led to chromosome fragmentation strikingly similar to that seen when cdc17+, the DNA ligase I gene, is inactivated. The temperature-dependent lethality of dna2 (ts) mutants was suppressed by overexpression of genes encoding subunits of polymerase δ (cdc1+ and cdc27+), DNA ligase I (cdc17+), and Fen-1 (rad2+). Each of these gene products plays a role in the elongation or maturation of Okazaki fragments. Moreover, they all interacted with S. pombe Dna2 in a yeast two-hybrid assay, albeit to different extents. On the basis of these results, we conclude that dna2+ plays a direct role in the Okazaki fragment elongation and maturation. We propose that dna2+ acts as a central protein to form a complex with other proteins required to coordinate the multienzyme process for Okazaki fragment elongation and maturation." @default.
- W1774053018 created "2016-06-24" @default.
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- W1774053018 date "2000-07-01" @default.
- W1774053018 modified "2023-09-26" @default.
- W1774053018 title "Genetic Analyses of <i>Schizosaccharomyces pombe dna2</i>+ Reveal That Dna2 Plays an Essential Role in Okazaki Fragment Metabolism" @default.
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- W1774053018 doi "https://doi.org/10.1093/genetics/155.3.1055" @default.
- W1774053018 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/1461167" @default.
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