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首页> 外文期刊>Molecular cell >miR-14 Regulates Autophagy during Developmental Cell Death by Targeting ip3-kinase 2
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miR-14 Regulates Autophagy during Developmental Cell Death by Targeting ip3-kinase 2

机译：miR-14通过靶向ip3-激酶2调节发育细胞死亡期间的自噬

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摘要

Macroautophagy (autophagy) is a lysosome-depen-dent degradation process that has been implicated in age-associated diseases. Autophagy is involved in both cell survival and cell death, but little is known about the mechanisms that distinguish its use during these distinct cell fates. Here, we identify the micro-RNA miR-14 as being both necessary and sufficient for autophagy during developmentally regulated cell death in Drosophila. Loss of miR-14 prevented induction of autophagy during salivary gland cell death, but had no effect on starvation-induced autophagy in the fat body. Moreover, misexpression of miR-14 was sufficient to prematurely induce autophagy in salivary glands, but not in the fat body. Importantly, miR-14 regulates this context-specific autophagy through its target, inositol 1,4,5-trisphos-phate kinase 2 {jp3k2), thereby affecting inositol 1,4,5-trisphosphate (IP3) signaling and calcium levels during salivary gland cell death. This study provides in vivo evidence of microRNA regulation of autophagy through modulation of IP3 signaling.
机译：巨自噬（自噬）是一种溶酶体依赖的降解过程，与年龄相关疾病有关。自噬与细胞存活和细胞死亡有关，但是对于在这些不同的细胞命运中区分其用途的机制知之甚少。在这里，我们确定果蝇中发育调控的细胞死亡过程中自噬的必要性和充分性的微小RNA miR-14。 miR-14的丢失阻止了唾液腺细胞死亡期间自噬的诱导，但对饥饿引起的脂肪体内自噬没有影响。此外，miR-14的错误表达足以在唾液腺中过早诱导自噬，但在脂肪体内则不能。重要的是，miR-14通过其靶标肌醇1,4,5-三磷酸磷酸盐激酶2（jp3k2）调节这种特定于上下文的自噬，从而影响唾液中肌醇1,4,5-三磷酸（IP3）信号传导和钙水平腺细胞死亡。这项研究提供了体内IP信号通过调节IP3信号的微RNA调节的证据。

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