Kang H Y, Choi E, Bae S H, Lee K H, Gim B S, Kim H D, Park C, MacNeill S A, Seo Y S
National Creative Research Initiative Center for Cell Cycle Control, Samsung Biomedical Research Institute, Sungkyunkwan University School of Medicine, Changan-Ku Suwon, Kyunggi-Do, 440-746, Korea.
Genetics. 2000 Jul;155(3):1055-67. doi: 10.1093/genetics/155.3.1055.
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 delta (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.
在本报告中,我们研究了粟酒裂殖酵母dna2(+)的温度敏感(ts)突变等位基因所导致的表型,dna2(+)是芽殖酵母DNA2的同源物,目的是在细胞周期S期滞后链合成方面进一步确定其在体内的功能。在限制温度下,dna2(ts)细胞停滞在S期后期,但总体DNA合成未受影响。此外,当与检查点突变结合时,它们表现出异常的有丝分裂,这与Dna2在冈崎片段成熟中的作用一致。同样,dna2(+)被破坏的孢子在萌发过程中复制了它们的DNA含量,也停滞在S期后期。dna2(+)的失活导致染色体片段化,与DNA连接酶I基因cdc17(+)失活时观察到的情况极为相似。dna2(ts)突变体的温度依赖性致死性被编码聚合酶δ亚基(cdc1(+)和cdc27(+))、DNA连接酶I (cdc17(+))和Fen-1 (rad2(+))的基因的过表达所抑制。这些基因产物中的每一个都在冈崎片段的延伸或成熟中发挥作用。此外,在酵母双杂交试验中,它们都与粟酒裂殖酵母Dna2相互作用,尽管程度不同。基于这些结果,我们得出结论,dna2(+)在冈崎片段的延伸和成熟中起直接作用。我们提出,dna2(+)作为一种核心蛋白,与协调冈崎片段延伸和成熟的多酶过程所需的其他蛋白形成复合物。