Bi Xiaolin, Wei Su-Chin D, Rong Yikang S
Laboratory of Molecular Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Curr Biol. 2004 Aug 10;14(15):1348-53. doi: 10.1016/j.cub.2004.06.063.
The conserved ATM checkpoint kinase and the Mre11 DNA repair complex play essential and overlapping roles in maintaining genomic integrity. We conducted genetic and cytological studies on Drosophila atm and mre11 knockout mutants and discovered a telomere defect that was more severe than in any of the non-Drosophila systems studied. In mutant mitotic cells, an average of 30% of the chromosome ends engaged in telomere fusions. These fusions led to the formation and sometimes breakage of dicentric chromosomes, thus starting a devastating breakage-fusion-bridge cycle. Some of the fusions depended on DNA ligase IV, which suggested that they occurred by a nonhomologous end-joining (NHEJ) mechanism. Epistasis analyses results suggest that ATM and Mre11 might also act in the same telomere maintenance pathway in metazoans. Since Drosophila telomeres are not added by a telomerase, our findings support an additional role for both ATM and Mre11 in telomere maintenance that is independent of telomerase regulation.
保守的ATM检查点激酶和Mre11 DNA修复复合体在维持基因组完整性方面发挥着重要且重叠的作用。我们对果蝇atm和mre11基因敲除突变体进行了遗传学和细胞学研究,发现了一种比任何已研究的非果蝇系统都更严重的端粒缺陷。在突变的有丝分裂细胞中,平均30%的染色体末端参与了端粒融合。这些融合导致了双着丝粒染色体的形成,有时还会断裂,从而启动了一个毁灭性的断裂-融合-桥循环。一些融合依赖于DNA连接酶IV,这表明它们是通过非同源末端连接(NHEJ)机制发生的。上位性分析结果表明,ATM和Mre11在多细胞动物中可能也作用于同一条端粒维持途径。由于果蝇端粒不是由端粒酶添加的,我们的发现支持了ATM和Mre11在端粒维持中具有独立于端粒酶调控的额外作用。