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首页> 外文期刊>The Journal of biological chemistry >EDD, a Ubiquitin-protein Ligase of the N-end Rule Pathway, Associates with Spindle Assembly Checkpoint Components and Regulates the Mitotic Response to Nocodazole *
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EDD, a Ubiquitin-protein Ligase of the N-end Rule Pathway, Associates with Spindle Assembly Checkpoint Components and Regulates the Mitotic Response to Nocodazole *

机译：EDD，N末端规则途径的泛素蛋白质连接酶，与主轴组件检查点组分相关联，并调节对Nocodazole的有丝分裂响应 *

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Background: Mitotic progression is regulated by the spindle assembly checkpoint (SAC) to prevent aneuploidy and chromosome damage. Results: EDD binds to various SAC components, governs the expression levels of key mitosis-associated proteins, and mediates the response to the mitotic spindle poison nocodazole. Conclusion: EDD contributes to the ability of the SAC to mediate checkpoint arrest. Significance: EDD may act to maintain genomic integrity. In this work, we identify physical and genetic interactions that implicate E3 identified by differential display (EDD) in promoting spindle assembly checkpoint (SAC) function. During mitosis, the SAC initiates a mitotic checkpoint in response to chromosomes with kinetochores unattached to spindle pole microtubules. Similar to Budding uninhibited by benzimidazoles-related 1 (BUBR1 ) siRNA, a bona fide SAC component, EDD siRNA abrogated G_(2)/M accumulation in response to the mitotic destabilizing agent nocodazole. Furthermore, EDD siRNA reduced mitotic cell viability and, in nocodazole-treated cells, increased expression of the promitotic progression protein cell division cycle 20 (CDC20). Copurification studies also identified physical interactions with CDC20, BUBR1, and other components of the SAC. Taken together, these observations highlight the potential role of EDD in regulating mitotic progression and the cellular response to perturbed mitosis.
机译：背景：纺织组件检查点（SAC）调节有丝分裂进展，以防止随风倍性和染色体损伤。结果：EDD与各种囊组分结合，治理关键有丝裂菌相关蛋白的表达水平，并介导对有丝分裂主轴毒毒臭氧唑的反应。结论：EDD有​​助于SAC调解检查点逮捕的能力。意义：EDD可以采取行动以维持基因组完整性。在这项工作中，我们识别通过在促进主轴组件检查点（SAC）功能方面通过差分显示器（EDD）识别的E3来识别E3的物理和遗传相互作用。在有丝分裂期间，囊响应于染色体的染色体引发有丝分子检查点，以与主轴杆微管的脊髓卷中的kinetochores。与苯并咪唑相关的1（BUBR1）siRNA不难抵消的芽，一个真囊囊组分，EDD siRNA废除G_（2）/ m响应于有丝分裂稳定剂Nocodazole而积累。此外，EDD siRNA降低了有丝分裂细胞活力，并且在Nocodazole处理的细胞中，增加了促进进展蛋白细胞分裂周期20的表达增加（CDC20）。复制研究还确定了与CDC20，BUBR1和囊的其他组分的物理相互作用。在一起，这些观察结果突出了EDD在调节有丝分裂进展和对扰动有丝分裂的细胞反应中的潜在作用。

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