Functional characterization of the InR/PI3K/AKT signaling pathway in female reproduction of the predatory bug Cyrtorhinus lividipennis (Hemiptera: Miridae)

Author:

Hu Kui1,Jin Rong1,Liu Jianqi1,Zhu Jun1,Dai Wei1,Wang Ying1,Li Yao1,Liu Fang123ORCID

Affiliation:

1. College of Plant Protection, Yangzhou University , Yangzhou 225009, China

2. Jiangsu Co-Innovation Center for Modern Production Technology of Grain Crops, Yangzhou University , Yangzhou 225009, China

3. Joint International Research Laboratory of Agriculture & Agri-Product Safety (Yangzhou University) , Jiangsu , Yangzhou 225009, China

Abstract

Abstract The insulin signaling (IIS) pathway plays a key role in the regulation of various physiological functions in animals. However, the involvement of IIS pathway in the reproduction of natural enemy insects remains enigmatic. Here, 3 key genes (named ClInR, ClPI3K, and ClAKT) related to IIS pathway were cloned from Cyrtorhinus lividipennis (Reuter) (Hemiptera: Miridae), an important natural enemy in the rice ecosystem. These 3 proteins had the typical features of corresponding protein families and shared high similarity with their respective homologs from the Hemipteran species. The ClInR, ClPI3K, and ClAKT were highly expressed in the adult stage. Tissue distribution analysis revealed that ClInR, ClPI3K, and ClAKT were highly expressed in the midgut and ovary of adults. Silencing of ClInR, ClPI3K, and ClAKT caused 92.1%, 72.1%, and 57.8% reduction in the expression of ClVg, respectively. Depletion of these 3 genes impaired vitellogenin synthesis and ovary development. Moreover, the fecundity in the dsInR, dsPI3K, and dsAKT injected females were 53.9%, 50.8%, and 48.5% lower than the control treatment, respectively. These results indicated that ClInR, ClPI3K, and ClAKT are of great importance for the reproduction of C. lividipennis. Our results advance the knowledge about the molecular mechanism of reproduction regulation in natural enemy insects.

Funder

National Natural Science Foundation of China

Publisher

Oxford University Press (OUP)

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