Journal
PLOS PATHOGENS
Volume 17, Issue 8, Pages -Publisher
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.ppat.1009846
Keywords
-
Categories
Funding
- Swiss National Science Foundation, Sinergia [CRSII5_186397]
- Novartis Foundation [532114]
- NIH [GM050545]
- Swiss National Science Foundation (SNF) [CRSII5_186397] Funding Source: Swiss National Science Foundation (SNF)
Ask authors/readers for more resources
The fruit fly Drosophila melanogaster produces a variety of effector peptides to combat microbial infection, including a novel antifungal peptide gene named Baramicin A. This gene is strongly induced in the fat body downstream of the Toll pathway and plays a key role in the antimicrobial response of the fruit fly.
The fruit fly Drosophila melanogaster combats microbial infection by producing a battery of effector peptides that are secreted into the haemolymph. Technical difficulties prevented the investigation of these short effector genes until the recent advent of the CRISPR/CAS era. As a consequence, many putative immune effectors remain to be formally described, and exactly how each of these effectors contribute to survival is not well characterized. Here we describe a novel Drosophila antifungal peptide gene that we name Baramicin A. We show that BaraA encodes a precursor protein cleaved into multiple peptides via furin cleavage sites. BaraA is strongly immune-induced in the fat body downstream of the Toll pathway, but also exhibits expression in other tissues. Importantly, we show that flies lacking BaraA are viable but susceptible to the entomopathogenic fungus Beauveria bassiana. Consistent with BaraA being directly antimicrobial, overexpression of BaraA promotes resistance to fungi and the IM10-like peptides produced by BaraA synergistically inhibit growth of fungi in vitro when combined with a membrane-disrupting antifungal. Surprisingly, BaraA mutant males but not females display an erect wing phenotype upon infection. Here, we characterize a new antifungal immune effector downstream of Toll signalling, and show it is a key contributor to the Drosophila antimicrobial response.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available