Drosophila caspase transduces Shaggy/GSK-3β kinase activity in neural precursor development
Drosophila caspase transduces Shaggy/GSK-3β kinase activity in neural precursor development
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DOI：
10.1038/sj.emboj.7600822
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发表时间：
2005-11-02
期刊：
影响因子：
11.4
通讯作者：
Miura, M
中科院分区：
文献类型：
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作者：
Kanuka, H;Kuranaga, E;Miura, M
半胱氨酸天冬氨酸氨基转移酶因其在细胞凋亡过程中的作用而广为人知，在该过程中，它们切割特定的靶蛋白，导致细胞的消除，以及它们在细胞因子成熟过程中的作用。在这项研究中，我们发现了一种新的底物，通过caspase的切割，可以调节果蝇神经前体的发育。Shaggy(SGG)46蛋白是由SGG基因编码的一种异构体，对无翅信号的负调控是必不可少的，它被黑暗依赖的caspase所切割。这种裂解将其转化为活性激酶，从而促进神经前体(感觉器官前体(SOP))细胞的形成。我们的证据表明，caspase对无翼途径的调控与细胞凋亡无关。这些结果暗示了caspase在神经前体发育中通过底物裂解调节细胞信号通路中的一个新的作用。
Caspases are well known for their role in the execution of apoptotic programs, in which they cleave specific target proteins, leading to the elimination of cells, and for their role in cytokine maturation. In this study, we identified a novel substrate, which, through cleavage by caspases, can regulate Drosophila neural precursor development. Shaggy (Sgg)46 protein, an isoform encoded by the sgg gene and essential for the negative regulation of Wingless signaling, is cleaved by the Dark-dependent caspase. This cleavage converts it to an active kinase, which contributes to the formation of neural precursor (sensory organ precursor (SOP)) cells. Our evidence suggests that caspase regulation of the wingless pathway is not associated with apoptotic cell death. These results imply a novel role for caspases in modulating cell signaling pathways through substrate cleavage in neural precursor development.