Can natural variation in Diptericin explain phylogenetic effects in resistance to bacteria infection?

• Grant number: 24/13788-0
• Support Opportunities: Scholarships abroad - Research Internship - Doctorate (Direct)
• Start date: December 01, 2024
• End date: November 30, 2025
• Field of knowledge: Biological Sciences - Genetics - Animal Genetics
• Principal Investigator: Rodrigo Cogni
• Grantee: Eduardo Gomes Ragnoni
• Supervisor: Mark Austin Hanson
• Host Institution: Instituto de Biociências (IB). Universidade de São Paulo (USP). São Paulo , SP, Brazil
• Institution abroad: University of Exeter, Penryn, England
• Associated to the scholarship: 22/09752-4 - Pathogen host shift: meta-analytical and experimental approaches using bacteria and insects interactions, BP.DD

Abstract

Emerging Infectious Diseases (EIDs) cause enormous negative effects in humanity and are becoming more frequent. One of the main sources of EIDs is host shift events (the jump of a pathogen from one host species to another). The host phylogeny can play a big role in the host shift success. One key model in host shift studies is the Drosophilidae family of flies. In my PhD we cross infected the bacteria P. rettgeri and E. faecalis originally from D. melanogaster to 38 other fly species of the Drosophilidae family and found that a great part of the variation of susceptibility to P. rettgeri infection can be explained by the phylogeny of the host (but not for other bacteria species). Hanson et al. 2023 suggested that the antimicrobial peptide Diptericin A (DptA) is responsible for the resistance against P. rettgeri infection, specifically the variation of the DptAS69 allele across species. In collaboration with Hanson's Lab (University of Exeter, U.K.) we intend to make and use mutant flies expressing heterologously variations of DptA and DptB proteins that are present in different species of the genus Drosophila inserted in the same genotype of D. melanogaster to answer the questions: What is the effect of each protein variation on the flies fitness against the P. rettgeri bacterium in vivo and ex vivo? How potent are the antibacterial properties of each protein against P. rettgeri and other bacteria species? Can these proteins explain the phylogenetic effects in our cross-infection experiments? This research will help to elucidate the causative factors behind the phylogeny in host shift and shed light on how EIDs arise from host shift on new species.