Effects of microbial infection on key gene expression in the Toll signaling pathway and immune response in Myzus persicae.

Pestic Biochem Physiol

Institute of Entomology, Guizhou University, Guizhou Key Laboratory of Agricultural Biosecurity, Guiyang 550025, China.

Published: November 2025


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Article Abstract

The Toll signaling pathway serves as a crucial regulatory mechanism in the insect innate immune system, playing a pivotal role in defending against pathogenic microorganisms. However, the specific functions of aphids' unique immune system and Toll signaling pathway remain poorly understood. In this study, we systematically analyzed 12 key genes associated with the Toll signaling pathway in Myzus persicae. Our findings revealed that Toll pathway-related genes exhibit high expression levels in the hemolymph and midgut tissues of the M. persicae. Furthermore, these genes were significantly upregulated following exposure to Staphylococcus aureus, Escherichia coli, and Beauveria bassiana. Through RNA interference (RNAi) coupled with microbial infection assays, we demonstrated that knockdown of Toll pathway-related genes substantially compromised the antibacterial capacity of M. persicae. Notably, we identified distinct functional specializations among these genes: MpMyd88 and MpIRAK4 were critical for resistance against S. aureus infection, while MpPelle, MpP38, MpJNK, and MpAP primarily mediated defense against B. bassiana. Additionally, genetic knockdown experiments revealed that MpMyd88, MpIRAK4, MpPelle, and MpCactus significantly downregulated the expression of key immune factors (MpNedd8, MpLys1, MpLys2, and MpLys3), though interestingly not MpPPO1 and MpPPO2. These results not only underscore the vital role played by the Toll signaling pathway in aphid immune defense but also provide essential molecular targets along with theoretical support for developing innovative aphid control strategies based on synergistic effects between RNAi and microbial.

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http://dx.doi.org/10.1016/j.pestbp.2025.106611DOI Listing

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