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母源-合子转换过程中 Cdc25 降解的结构-功能分析。

Structure-function analysis of Cdc25 degradation at the maternal-to-zygotic transition.

机构信息

Department of Cell Biology, Duke University Medical Center, Durham, NC, USA.

Department of Surgery, Alpert Medical School, Brown University, Providence, RI, USA.

出版信息

Fly (Austin). 2022 Dec;16(1):111-117. doi: 10.1080/19336934.2022.2043095.

Abstract

Downregulation of protein phosphatase Cdc25 activity is linked to remodelling of the cell cycle during the maternal-to-zygotic transition (MZT). Here, we present a structure-function analysis of Cdc25. We use chimeras to show that the N-terminus regions of Cdc25 and Cdc25 control their differential degradation dynamics. Deletion of different regions of Cdc25 reveals a putative domain involved in and required for its rapid degradation during the MZT. Notably, a very similar domain is present in Cdc25 and deletion of the DNA replication checkpoint results in similar dynamics of degradation of both Cdc25 and Cdc25. Finally, we show that Cdc25 degradation is delayed in embryos lacking the left arm of chromosome III. Thus, we propose a model for the differential regulation of Cdc25 at the MZT.

摘要

蛋白磷酸酶 Cdc25 活性的下调与母源至合子过渡(MZT)期间细胞周期的重塑有关。在这里,我们对 Cdc25 进行了结构功能分析。我们使用嵌合体表明 Cdc25 和 Cdc25 的 N 端区域控制它们的差异降解动力学。Cdc25 的不同区域的缺失揭示了一个可能的参与并需要其在 MZT 期间快速降解的结构域。值得注意的是,Cdc25 和 Cdc25 中存在一个非常相似的结构域,删除 DNA 复制检查点会导致这两种 Cdc25 的降解动力学相似。最后,我们表明,在缺乏染色体 III 左臂的胚胎中,Cdc25 的降解会延迟。因此,我们提出了一个在 MZT 中对 Cdc25 进行差异调节的模型。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b24b/8890428/0d18adc2b4ed/KFLY_A_2043095_F0001_OC.jpg

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