Fights on the surface prior to fungal invasion of insects.

Entomopathogenic fungi (EPF) infect insects by landing on and penetrating cuticles. Emerging evidence has shown that, prior to the invasion of insects, fungal cells have to battle and overcome diverse challenges, including the host behavioral defenses, colonization resistance mediated by ectomicrobiotas, host recognition, and generation of enough penetration pressure. The ascomycete EPF such as Metarhizium and Beauveria can thus produce adhesive proteins and/or the exopolysaccharide mucilage to tightly glue fungal cells on cuticles. Producing antimicrobial peptides and chemical compounds can enable EPF to outcompete cuticular defensive microbes. The use of divergent membrane receptors, accumulation, and quick degradation of lipid droplets in conidial cells can help EPF recognize proper hosts and build up cellular turgor to breach cuticles for systematic invasion. Further investigations are still required to unveil the multifaceted and intricate relationships between EPF and insect hosts.

Suppression of Drosophila antifungal immunity by a parasite effector via blocking GNBP3 and GNBP-like 3, the dual receptors for ß-glucans.

The tactics used by animal pathogens to combat host immunity are largely unclear. Here, we report the depiction of the virulence-required effector Tge1 deployed by the entomopathogen Metarhizium robertsii to suppress Drosophila antifungal immunity. Tge1 can target both GNBP3 and GNBP-like 3 (GL3), and the latter can bind to ß-glucans like GNBP3, whereas the glucan binding by both receptors can be attenuated by Tge1. As opposed to the surveillance GNBP3, GL3 is inducible in Drosophila depending on the Toll pathway via a positive feedback loop mechanism. Losses of GNBP3 and GL3 genes result in the deregulations of protease cascade, Spätzle maturation, and antimicrobial gene expressions in Drosophila upon fungal challenges. Fly survival assays confirm that GL3 plays a more essential role than GNBP3 in combating fungal infections. In addition to evidencing the gene-for-gene interactions between fungi and insects, our data advance insights into Drosophila antifungal immunity.