Uncovering the function of insulin receptor substrate in termites’ immunity through active immunization

Author:

Zhou Wei1,Zhao Xingying1,Hassan Ali1,Jia Bao12,Liu Long3,Huang Qiuying1ORCID

Affiliation:

1. Hubei Insect Resources Utilization and Sustainable Pest Management Key Laboratory, Huazhong Agricultural University , Wuhan 430070 , China

2. Nanning Institute of Termite Control , Nanning 530023 , China

3. Henan International Laboratory for Green Pest Control, Henan Engineering Laboratory of Pest Biological Control, College of Plant Protection, Henan Agricultural University , Zhengzhou 450002 , China

Abstract

Abstract Insulin receptor substrate (IRS) proteins are key mediators in insulin signaling pathway. In social insect lives, IRS proteins played important roles in caste differentiation and foraging, but there function in disease defenses such as active immunization has not been reported yet. To investigate the issue, we successfully suppressed the IRS gene 3 days after dsRNA injection. Suppressing IRS gene increased the contents of glucose, trehalose, glycogen, and triglyceride and decreased the content of pyruvate in termites, and led to the metabolic disorder of glucose and lipids. IRS suppressing significantly enhanced grooming behaviors of nestmates of fungus-contaminated termites and hence increased the conidial load in the guts of the nestmates. Additionally, IRS suppressing led to significant downregulation of the immune genes Gram-negative bacteria-binding protein2 (GNBP2) and termicin and upregulation of the apoptotic gene caspase8, and hence diminished antifungal activity of nestmates of fungus-contaminated termites. The above abnormal behavioral and physiological responses significantly decreased the survival rate of dsIRS-injected nestmates of the fungus-contaminated termites. These findings suggest that IRS is involved in regulation of active immunization in termites, providing a better understanding of the link between insulin signaling and the social immunity of termites.

Funder

National Natural Science Foundation of China

Publisher

Oxford University Press (OUP)

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