Drosophila's insulin/P13-kinase pathway coordinates cellular metabolism with nutritional conditions
Drosophila's insulin/P13-kinase pathway coordinates cellular metabolism with nutritional conditions
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DOI：
10.1016/s1534-5807(02)00117-x
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发表时间：
2002-02-01
影响因子：
11.8
通讯作者：
Edgar, BA
中科院分区：
文献类型：
--
作者：
Britton, JS;Lockwood, WK;Edgar, BA
在果蝇中的研究表明，胰岛素受体/磷脂酰肌醇3-激酶(INR/PI3K)信号是一种强大的细胞生长调节因子，但其在发育过程中的功能仍不确定。在这里，我们表明，抑制INR/PI3K信号表现出饥饿对细胞和组织的影响，而激活这一途径则绕过了细胞生长的营养需求，在生物水平上造成了饥饿敏感性。与这些发现一致的是，使用Pleckstrin同源结构域-绿色荧光蛋白(PH-GFP)融合作为PI3K活性指标的研究表明，PI3K受体内饮食蛋白可获得性的调节。因此，我们推测，果蝇体内胰岛素/PI3K信号的一个基本功能是协调细胞代谢和营养条件。
Studies in Drosophila have characterized insulin receptor/phosphoinositide 3-kinase (Inr/PI3K) signaling as a potent regulator of cell growth, but its function during development has remained uncertain. Here we show that inhibiting Inr/PI3K signaling phenocopies the cellular and organismal effects of starvation, whereas activating this pathway bypasses the nutritional requirement for cell growth, causing starvation sensitivity at the organismal level. Consistent with these findings, studies using a pleckstrin homology domain-green fluorescent protein (PH-GFP) fusion as an indicator for PI3K activity show that PI3K is regulated by the availability of dietary protein in vivo. Hence we surmise that an essential function of insulin/PI3K signaling in Drosophila is to coordinate cellular metabolism with nutritional conditions.