飞蝗对环境变化生殖适应的内分泌调控机制研究

Insects are characterized by their high fecundity, which is a strategy of insects to adapt environmental changes and a genetic basis of insect pest outbreak. However, the molecular mechanisms of high fecundity in insects are poorly understood. The migratory locust, a destructive insect pest, adapts to environmental changes by altering its fecundity including the number and size of eggs. Vitellogenin (Vg) required for locust egg maturation is synthesized in the fat body, released into the hemolymph and transported to maturing oocytes through the intercellular spaces (named patency) formed in the follicular epithelium. These processes are controlled by juvenile hormone (JH), but the underlying molecular mechanisms remain elusive. Based on our previous research and under the various nutrition and dry environment, we aim to：(1) elucidate how adult fat bodies undergo tissue and functional remodeling to become competent for Vg synthesis; (2) reveal the molecular mechanisms of JH action through crosstalking with insulin signaling and ployploidization for massive Vg synthesis; and (3) identify JH membrane receptor and explore how JH acts though the membrane signal transduction to initiate patency. The results will provide new insights into our understanding in the regulation of high fecundity and strong adaptability in locusts.

昆虫的强大生殖力是对环境变化的适应，也是害虫爆发成灾的遗传基础，但其分子调控机制尚有待深入阐明。飞蝗是重要的农业害虫，能够通过改变生殖力包括产卵量和卵的大小适应环境变化。已知飞蝗卵形成所需的卵黄原蛋白（Vg）由脂肪体合成并通过血淋巴和卵泡细胞间的通道（patency）运送到卵母细胞，促进卵的同步成熟，这些过程由保幼激素（JH）调节。但是，JH如何调控脂肪体中Vg的大量合成，如何调控patency的开关仍然不清楚。本项目拟在原有研究基础上，通过改变飞蝗的营养和干燥环境，（1）剖析成虫脂肪体通过细胞增殖与分化进行组织和功能重塑的分子机理；（2）阐明JH通过与胰岛素信号交流和细胞多倍化促进Vg大量合成的分子调控机制；（3）鉴定JH的膜受体，揭示JH通过膜信号传递启动patency的分子开关。本研究对于了解飞蝗繁殖量大和环境适应性强的生物学基础具有重要的科学意义。

昆虫的强大生殖力是对环境变化的适应，也是害虫种群暴发的生物学基础。飞蝗是重要的农业害虫，保幼激素（JH）调控其卵黄原蛋白（Vg）在脂肪体合成、通过卵泡细胞间通道（patency）运输到卵母细胞、然后经VgR介导的内吞作用进入卵母细胞，但其中的分子机制尚不清楚。本项目主要研究JH调控脂肪体发育、Vg在脂肪体合成以及Vg在卵巢运输的分子机制。发现JH通过含INDEL/PRD结构域的可变剪切体Tai-A增强在脂肪体的基因调控功能，提升Vg合成能力。解析了JH激发Grp78-1和Grp78-2表达维持脂肪体细胞稳态，以及诱导Greglin表达抑制丝氨酸类蛋白酶活性，进而保障脂肪体Vg合成能力的机制。阐释了JH通过PKCα磷酸化Kr-h1招募激活因子CBP，上调核糖体基因RL36表达，进而促进Vg合成的机制。探究了JH通过Met/Tai上调内分裂基因Cdk6和E2f1表达，促进脂肪体细胞多倍化和Vg合成的机制。揭示了JH通过GPCR/RTK-PLC-IP3R-PKC通路激活Na+/K+-ATPase，开启卵泡细胞间通道将Vg运输到卵母细胞，再经GPCR-PLC-PKCι途径磷酸化VgR并激活VgR介导的内吞作用，运送Vg进入卵母细胞的机制。在PNAS、BMC Biology、Cellular and Molecular Life Sciences、Development、Journal of Biological Chemistry、The FASEB Journal、Insect Biochemistry and Molecular Biology等国际知名期刊发表论文13篇，较好完成了研究目标，超额完成了预期成果，丰富了对JH调控昆虫生殖的分子机制的了解，为害虫防治提供了潜在分子靶标。通过本项目研究，我们在昆虫生殖的激素调控领域形成了明显的特色优势，得到了国内外领域同行的认可。