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Knockdown of FAS2 Impairs Fecundity by Inhibiting Lipid Accumulation and Increasing Glycogen Storage in Locusta
Jiaying Xu1, Ya Tang1, Yi Jin1
1College of life and Environmental Sciences, Hangzhou Normal University, Hangzhou 311121, China.
Abstract:
Fatty acid synthase (FAS) is a pivotal gene in the lipid synthesis pathway and plays a crucial role in insect energy metabolism. Locusta migratoria, as one of the major agricultural pests, requires identification of new targets to control or reduce its reproductive capacity for effective locust pest management strategies. In this study, we focused on L. migratoria and identified FAS2 as a potential target gene with functional significance in lipid metabolism and reproduction based on sequence characteristics analysis and tissue-expression patterns of five FAS genes. Subsequently, through RNA interference (RNAi) targeting FAS2 expression, we assessed alterations in lipid and carbohydrate metabolism-related gene expression levels, lipid and carbohydrate contents, ovarian development, and reproductive capacity using experimental techniques such as RT-qPCR, ELISA, and morphological observations. Our findings revealed that interference with FAS2 upregulated genes involved in lipid degradation, including Lsd-1, Lsd-2, Lipase3, and Brummer, while significantly decreasing the TAG content and fat accumulation. At the level of carbohydrate metabolism, FAS2 silencing led to significant upregulation of key genes TPS and GS in the synthesis pathway, resulting in increased glycogen and trehalose content. In addition, FAS2 interference resulted in a significant reduction of Vg mRNA expression level sand protein content in L. migratoria, followed by delayed ovarian development and reduced egg production. This further confirms that impaired FAS2 function prompts L. migratoria to enhance lipid degradation and sugar storage to maintain the energy balance, while reducing the energy investment into reproduction. Collectively, the results of this study suggest that FAS2 can serve as a novel molecular target for controlling L. migratoria.
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