Correlative analysis of transcriptome and 16S rDNA in Procambarus clarkii reveals key signaling pathways are involved in Chlorantraniliprole stress response by phosphoinositide 3-kinase (PI3K)

克氏原螯虾 转录组 信号转导 PI3K/AKT/mTOR通路 生物 相关 磷酸肌醇3激酶 计算生物学 钥匙(锁) 细胞生物学 遗传学 基因 生态学 基因表达 小龙虾 语言学 哲学
作者
Dandan Bian,Xin Liu,Xue Jun Zhang,Geng-Yu Zhang,Ren-Chao Wu,Yan-Xia Shi,Xi-Rong Zhu,Dai-Zhen Zhang,Qiu-Ning Liu,Boping Tang,Baojian Zhu
出处
期刊:International Journal of Biological Macromolecules [Elsevier BV]
卷期号:: 135966-135966
标识
DOI:10.1016/j.ijbiomac.2024.135966
摘要

Chlorantraniliprole (CAP), a diamide insecticide, is extensively used in agricultural production. With the increasing adoption of the rice-crayfish integrated farming model, pesticide application has become more frequent. However, the potential risk of CAP to crayfish (Procambarus clarkii) remains unclear. In this study, crayfish were exposed to 30, 60, 90 mg/L CAP for 96 h. As CAP exposure time and concentration increased, crayfish survival rates and total hemocyte counts (THC) decreased. Biochemical indicators revealed that CAP exposure induced oxidative stress and immunosuppression in crayfish, leading to metabolic disorders and reduced ATP content. Additionally, pathological analysis and 16S rDNA sequencing demonstrated that CAP exposure compromised the intestinal barrier of crayfish, altered the intestinal microbial community structure, and caused apoptosis. Differential gene expression analysis showed that CAP exposure significantly suppressed the expression of genes related to immune and energy metabolism pathways, resulting in immune dysfunction and insufficient energy supply, while activating the PI3K/AKT/mTOR signaling pathway. PI3K knockdown reduced antioxidant and digestive activities, increased the expression of proinflammatory and apoptosis genes, and exacerbated CAP-induced intestinal toxicity. This study is the first to explore the characterization and function of PI3K in crustaceans, providing new insights for further research on crustacean antioxidants and defense mechanisms.
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