Jin Ke-Yan, Di Yu-Qin, Liu Tian-Wen, Zhao Xiao-Fan
Shandong Provincial Key Laboratory of Animal Cells and Developmental Biology, School of Life Sciences, Shandong University, Qingdao, 266237, Shandong Province, China.
Insect Sci. 2025 Jun;32(3):899-911. doi: 10.1111/1744-7917.13438. Epub 2024 Aug 26.
The fat body of the holometabolous insect is remodeled by the degradation of the larval fat body and the development of the adult fat body during metamorphosis. However, the mechanism of adult fat body development is quite unclear. Using the agricultural pest Helicoverpa armigera, the cotton bollworm, as a model, we revealed that the development of adult fat body was regulated by glycolysis, triglyceride (triacylglycerol [TAG]) synthesis, cell proliferation, and cell adhesion. RNA sequencing detected a set of genes that were upregulated in the 8-d late pupal fat body at a late metamorphic stage compared with the 2-d pupal fat body at an earlier metamorphic stage. The pathways for glycolysis, TAG synthesis, cell proliferation, and cell adhesion were enriched by the differentially expressed genes, and the key genes linked with these pathways showed increased expression in the 8-d pupal fat body. Knockdown of phosphofructokinase (Pfk), acetyl-CoA carboxylase (Acc1), phosphatidylinositol 4,5-bisphosphate 3-kinase catalytic subunit (P110) and collagen alpha-1(IV) chain (Col4a1) by RNA interference resulted in abnormal eclosion and death at pupal stages, and repressed lipid droplets accumulation and adult fat body development. The expression of Acc1, P110, and Col4a1 was repressed by the insect steroid hormone 20-hydroxyecdysone (20E). The critical genes in the 20E pathway appeared to decrease at the late pupal stage. These data suggested that the development of the insect adult fat body is regulated by glycolysis, lipids synthesis, cell proliferation, and cell adhesion at the late pupal stage when the 20E signal decreases.
全变态昆虫的脂肪体在变态过程中通过幼虫脂肪体的降解和成虫脂肪体的发育而重塑。然而，成虫脂肪体发育的机制尚不清楚。以农业害虫棉铃虫为模型，我们发现成虫脂肪体的发育受糖酵解、甘油三酯（三酰甘油 [TAG]）合成、细胞增殖和细胞黏附的调控。RNA 测序检测到一组基因，与变态早期 2 日龄蛹脂肪体相比，在变态晚期 8 日龄蛹脂肪体中上调。糖酵解、TAG 合成、细胞增殖和细胞黏附途径被差异表达基因富集，与这些途径相关的关键基因在 8 日龄蛹脂肪体中表达增加。通过 RNA 干扰敲低磷酸果糖激酶（Pfk）、乙酰辅酶 A 羧化酶（Acc1）、磷脂酰肌醇 4,5-二磷酸 3-激酶催化亚基（P110）和胶原蛋白α-1(IV)链（Col4a1）导致蛹期羽化异常和死亡，并抑制脂滴积累和成虫脂肪体发育。Acc1、P110 和 Col4a1 的表达受昆虫类固醇激素 20-羟基蜕皮激素（20E）抑制。20E 信号通路中的关键基因在蛹后期似乎减少。这些数据表明，在 20E 信号降低的蛹后期，昆虫成虫脂肪体的发育受糖酵解、脂质合成、细胞增殖和细胞黏附的调控。
