Abstract
Pseudomonas entomophila is an entomopathogenic bacterium that infects and kills Drosophila. P. entomophila pathogenicity is linked to its ability to cause irreversible damages to the Drosophila gut, preventing epithelium renewal and repair. Here we report the identification of a novel pore-forming toxin (PFT), Monalysin, which contributes to the virulence of P. entomophila against Drosophila. Our data show that Monalysin requires N-terminal cleavage to become fully active, forms oligomers in vitro, and induces pore-formation in artificial lipid membranes. The prediction of the secondary structure of the membrane-spanning domain indicates that Monalysin is a PFT of the ß-type. The expression of Monalysin is regulated by both the GacS/GacA two-component system and the Pvf regulator, two signaling systems that control P. entomophila pathogenicity. In addition, AprA, a metallo-protease secreted by P. entomophila, can induce the rapid cleavage of pro-Monalysin into its active form. Reduced cell death is observed upon infection with a mutant deficient in Monalysin production showing that Monalysin plays a role in P. entomophila ability to induce intestinal cell damages, which is consistent with its activity as a PFT. Our study together with the well-established action of Bacillus thuringiensis Cry toxins suggests that production of PFTs is a common strategy of entomopathogens to disrupt insect gut homeostasis.
Highlights
The intestinal epithelium has a role in defining the barrier between the host and the external environment [1]
This is exemplified by fruit flies that live in rotting fruits and are capable of transmitting phytopathogenic bacteria
To study how pathogenic bacteria disrupt gut homeostasis, we investigated the interactions between Drosophila and a newly identified entomopathogen, Pseudomonas entomophila
Summary
The intestinal epithelium has a role in defining the barrier between the host and the external environment [1] This barrier protects the host against invasion and systemic dissemination of both pathogenic and commensal microorganisms. Both resistance and tolerance mechanisms contribute to maintain the gut integrity from the assault of infectious bacteria [2]. P. entomophila is able to persist in the Drosophila gut It induces the expression of antimicrobial peptide genes via the Imd pathway, both locally in the intestinal epithelium and systemically in the fat body, an organ analog to the mammalian liver [4]. The Gac system controls the production of a secreted protease, AprA, which is important for P. entomophila to counteract the local immune response of Drosophila [7]
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