DNA-replication/DNA-damage-dependent centrosome inactivation in Drosophila embryos
DNA-replication/DNA-damage-dependent centrosome inactivation in Drosophila embryos
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DOI：
10.1038/35000041
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发表时间：
2000-02-01
影响因子：
21.3
通讯作者：
Theurkauf, WE
中科院分区：
文献类型：
--
作者：
Sibon, OCM;Kelkar, A;Theurkauf, WE
在黑腹果蝇的早期胚胎发生过程中，dna复制检查点的突变导致染色体分离失败。在这里，我们发现这些分离失败与微管纺锤体的装配、中心体功能的有丝分裂特异性丧失以及核心中心体结构中γ -微管蛋白环复合物的几个组分的分离有关。DNA复制抑制剂aphidicolin和DNA损伤剂在野生型胚胎中触发相同的有丝分裂缺陷，表明中心体失活是对受损或不完全复制的DNA的检查点独立和有丝分裂特异性反应。我们提出中心体失活是损伤控制系统的一部分，当复制/损伤检查点控制失败时，中心体失活可以阻止染色体分离。
During early embryogenesis of Drosophila melanogaster, mutations in the DNA-replication checkpoint lead to chromosome-segregation failures. Here we show that these segregation failures are associated with the assembly of an anastral microtubule spindle, a mitosis-specific loss of centrosome function, and dissociation of several components of the gamma-tubulin ring complex from a core centrosomal structure. The DNA-replication inhibitor aphidicolin and DNA-damaging agents trigger identical mitotic defects in wild-type embryos, indicating that centrosome inactivation is a checkpoint-independent and mitosis-specific response to damaged or incompletely replicated DNA, We propose that centrosome inactivation is part of a damage-control system that blocks chromosome segregation when replication/damage checkpoint control fails.