Locust can detect β-1, 3-glucan of the fungal pathogen before penetration and defend infection via the Toll signaling pathway.

The timing and mechanism by which a host insect initiates an immune response are critical to successful defense against infection. Pathogen recognition, a prerequisite for host defense, has long been recognized to take place during the insect epidermis invasion by fungus. Here we report that insect can sense the fungal pathogen before host cuticle is penetrated by fungus. We discovered the upstream pattern recognition receptor (PRR) genes of the Toll pathway were upregulated in both the integument and fat body early during fungal germination on the epicuticle of Locusta migratoria manilensis. The Toll signaling pathway was strongly activated in the fat body at the penetration stage. RNAi of Myd88 increased the susceptibility of locusts to fungal infection, but that of Cactus showed the opposite effect. In addition, β-1, 3-glucan (laminarin), the main component of the cell wall of the pathogenic fungus Metarhizium acridum, was capable of activating the Toll signaling pathway (Spaetzle and Cactus) when it was applied on the host cuticle. These results demonstrate that host epidemis can effectively defend fungal infection by detecting β-1, 3-glucan on the fungal cell wall and activate the Toll signaling pathway even before fungal penetration.
Competing Interests: Declaration of competing interest This work was supported by grants from the Natural Science Foundation of China (No. 31540089) and Chongqing University Postgraduates’ Innovative Team Building Project (Team number: 200909B1009). The authors declare no financial and non-financial competing interests.
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