Abstract
Insect pathogens have adopted an array of mechanisms to subvert the immune pathways of their respective hosts. Suppression may occur directly at the level of host–pathogen interactions, for instance phagocytic capacity or phenoloxidase activation, or at the upstream signaling pathways that regulate these immune effectors. Insect pathogens of the family Baculoviridae, for example, are known to produce a UDP-glycosyltransferase (UGT) that negatively regulates ecdysone signaling. Normally, ecdysone positively regulates both molting and antimicrobial peptide production, so the inactivation of ecdysone by glycosylation results in a failure of host larvae to molt, and probably a reduced antimicrobial response. Here, we examine a putative ecdysteroid glycosyltransferase, Hba_07292 (Hb-ugt-1), which was previously identified in the hemolymph-activated transcriptome of the entomopathogenic nematode Heterorhabditis bacteriophora. Injection of recombinant Hb-ugt-1 (rHb-ugt-1) into Drosophila melanogaster flies resulted in diminished upregulation of antimicrobial peptides associated with both the Toll and Immune deficiency pathways. Ecdysone was implicated in this suppression by a reduction in Broad Complex expression and reduced pupation rates in r Hb-ugt-1-injected larvae. In addition to the finding that H. bacteriophora excreted-secreted products contain glycosyltransferase activity, these results demonstrate that Hb-ugt-1 is an immunosuppressive factor and that its activity likely involves the inactivation of ecdysone.
Highlights
Insect pathogens have adopted an array of mechanisms to subvert the immune pathways of their respective hosts
The genome of the nematode Pristionchus pacificus contains a putative ecdysone receptor homolog, and another has been postulated in H. bacteriophora, though this has yet to be confirmed[12]
In agreement with the RNA sequencing assay that initially identified this glycosyltransferase[13], Hb-ugt-1 was upregulated by H. bacteriophora infective juveniles (IJs) in response to hemolymph from multiple insect species, including D. melanogaster, though interestingly not in response to the nematode’s symbiotic bacterium Photorhabdus luminescens
Summary
Insect pathogens have adopted an array of mechanisms to subvert the immune pathways of their respective hosts. If this is the case, H. bacteriophora would require a negative regulatory element that is active against 20E to moderate its own development This molecule could function as a virulence factor similar to that of baculoviruses if it were secreted and diminished host 20E signaling. Expression of the transcription factor Broad Complex and molting ability were subsequently characterized following rHb-ugt-1 injection to determine whether ecdysone signaling might play a role in the observed AMP suppression. Both were significantly diminished, suggesting a decreased amount of active insect 20E after exposure to rHb-ugt-1. This collection of evidence is consistent with a role for Hb-ugt-1 as an ecdysone-inactivating virulence factor
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