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| Funder | Natural Environment Research Council |
|---|---|
| Recipient Organization | John Innes Centre |
| Country | United Kingdom |
| Start Date | Sep 30, 2023 |
| End Date | Mar 30, 2027 |
| Duration | 1,277 days |
| Number of Grantees | 2 |
| Roles | Student; Supervisor |
| Data Source | UKRI Gateway to Research |
| Grant ID | 2930381 |
Scientific background
Microbiomes offer great benefits to their hosts, including nutrient acquisition, growth promotion, immunity, and defence against disease but they are complex and difficult to study. As a result, insects have emerged as simple, experimentally tractable models with which to study microbiomes.
Our model is the leafcutter ant Acromyrmex echinatior, which has a simple cuticular microbiome dominated by antibiotic-producing bacteria that protect the ants against disease. The question in this project is how do the ants recruit antibiotic-producing (useful) bacteria while keeping out all other (cheater) bacteria?
Hypothesis: We know the ants pass a single strain of antibiotic-producing Pseudonocardia bacteria from generation to generation. Preliminary data suggest these are bacteriocin-type antibiotics. We have shown in vitro that this vertically transmitted strain could result in selective acquisition of antibiotic-producing Streptomyces bacteria, resulting in a defensive microbiome producing multiple types of antibiotics that is robust to the evolution of resistance by pathogens.
Antibiotic-producing bacteria are necessarily themselves antibiotic resistant and are pre-adapted to the Pseudonocardia-toxin-infused ant cuticle, allowing them to consume nutrients provided by the ants to their cuticular microbiome. Research methodology
The student will test the prediction that only antibiotic-producing bacteria that are resistant to Pseudonocardia antibiotics can colonise the ant cuticle, and this is why the ants are able to selectively recruit a microbiome dominated by Pseudonocardia and Streptomyces bacteria. This will involve: 1. Identifying the antibiotics made by the Pseudonocardia bacteria.
2. Testing them for activity against a range of different bacteria. 3. Determining their mode(s) of action. 4. Identifying the antibiotic resistance genes (ARGs) that make Streptomyces bacteria resistant.
John Innes Centre
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