The steroid hormone 20-hydroxyecdysone upregulates calcium release-activated calcium channel modulator 1 expression to induce apoptosis in the midgut of Helicoverpa armigera
The steroid hormone 20-hydroxyecdysone upregulates calcium release-activated calcium channel modulator 1 expression to induce apoptosis in the midgut of Helicoverpa armigera
复制标题
类固醇激素20-羟基蜕皮激素上调棉铃虫中肠钙释放激活钙通道调节因子1的表达诱导细胞凋亡
DOI：
10.1016/j.ceca.2017.10.004
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发表时间：
2017-12-01
期刊：
影响因子：
4
通讯作者：
Zhao, Xiao-Fan
中科院分区：
文献类型：
--
作者：
Li, Yong-Bo;Pei, Xu-Yang;Zhao, Xiao-Fan
Animal steroid hormones stimulate extracellular Ca2+ influx into cells; however, the mechanism remains unclear. In this study, we determined that the Ca2+ influx induced by steroid hormone 20-hydroxyecdysone (20E) is mediated by the calcium release-activated calcium channel modulator 1 (CRACM1/Orail). The Orail mRNA is highly expressed during midgut programmed cell death in the lepidopteran insect Helicoverpa armigera. 20E upregulated the expression of Orail in H. armigera larvae and in an epidermal cell line (HaEpi). Knockdown of Orail in HaEpi cells blocked 20E-induced Ca2+ influx, and the inhibitor of inositol 1, 4, 5-trisphosphate receptor (IP3R) Xestospongin (XeC) blocked 20E-induced Ca2+ influx, suggesting that 20E, via Orail, induces stored operated Ca2+ influx. Orail interacts with stromal interaction molecule 1(Stim1) to exert its function in 20E-induced Ca2+ influx. 20E promotes Orail aggregation through G-protein-coupled receptors, phospholipase C gamma 1, and Stiml. Knockdown of Orail in the HaEpi cell line repressed apoptosis and maintained autophagy under 20E regulation. Knockdown of Orail in larvae delayed pupation, repressed midgut apoptosis, maintained the midgut in an autophagic state, and repressed 20E-pathway gene expression. These results revealed that steroid hormone 20E, via Orail, induces Ca2+ influx to promote the transition of midgut from autophagy to apoptosis.
