It's in our genesThe lab has a core interest in studying the evolution of the immune system. We use a library of 50+ genome-sequenced fruit fly species as a model system for infection biology. By using fruit flies, we can probe questions in high-throughput, ethical, cost-effective, and genetically powerful ways. But the lab is also interested to study evolutionary questions more broadly, admittedly with a passion for insect genetics. The reason we study insects isn't arbitrary. See... vertebrates and mammals have both an adaptive and an innate immune system. However, insects have only an innate immune system. This is both a strength and a weakness for investigating immune evolution. While it means the questions we study are restricted to innate immunity, it also means we can do so with a clear signal, avoiding any statistical noise that comes from the host adaptive immune response. Insect genetics, and especially fruit fly genetics, are also immensely powerful. There are living libraries of flies where, at the click of a button, you can order tools for custom gene knockouts or overexpression in tissue-specific, timing-specific, heck... light-specific fashion. The lab is also regularly synthesizing plasmids and creating transgenic flies for our research purposes. When we have a hypothesis, we can typically test it in 3-4 different ways in a matter of weeks, generating high quality evidence. There is a reason Drosophila won the Nobel Prize in Physiology or Medicine in 2011, and again for founding the field of circadian biology in 2017: fruit flies are cool. While the lab has projects available using fruit fly research, there is also a general interest to study immune evolution more broadly. One species we are branching out into is Myzus persicae aphids, and in the past Mark has helped in placing the phylogenetics of stalked jellyfish (staurozoa, tiny but beautiful creatures). So if you are interested in some sort of evolutionary question, particularly (but not necessarily) involving host-pathogen interactions, please get in touch. Host-pathogen interactions in an evo-immunology contextSuitable for Masters, PhD, or Postdoctoral researchers  Immune genes evolve faster than almost any other gene in the genome. My work on antimicrobial peptides revealed how these host defence genes contribute to killing pathogens. What I found defied assumptions about immune defences that had held for decades, and blew the field of host peptide-pathogen evolutionary interactions wide open. These are still early days, but my work in the model fruit fly Drosophila melanogaster suggested that single peptides were immensely important for defence against specific microbes. What was striking was how you could delete entire groups of other defence peptides with no effect on survival outcome. In Hanson et al. (2023; Science, pdf here), I took this a step further, describing why these highly specific host effector-pathogen interactions exist: they're a product of millions of years of host evolution to ecological microbiome compositions. So these things I was seeing in the lab weren't just artefacts of our infection system, they reflected something ancient and meaningful. To date, my own work and the broader field of Drosophila immunity has described numerous highly-specific host peptide-microbe interactions. Yet the causative mechanisms remain poorly understood. It's also unclear how far beyond D. melanogaster one can trust a host-pathogen interaction to play by the same rules. And if different species do play by different rules, what are those rules? Are there signals we can look for to tell us when something is expected to behave the same or different from our classic model organism that we know so well? As the first line of defence against infection, and the core effectors that actually do the killing, antimicrobial peptides and other effector mechanisms (e.g. melanisation) are key arenas of host-pathogen evolution. There are so many observations to follow up on, and even genetic tools in the lab just waiting for a motivated student to use. Please reach out if you'd like to reveal some of the core principles of host-pathogen interactions using a powerful genetic model system. Characterising the immune repertoire of a global crop pest Myzus persicae aphidsSuitable for Masters, PhD, or Postdoctoral researchers
The lab has a number of projects related to Drosophila testacea genetics. This species has a fascinating and bizarre selfish chromosome, segregating genetic alleles, and a potential for truly impactful evolutionary biology tools at a fundamental level - and I'm not just saying that. These projects are suited for any level of investigation, from undergraduate term projects to enabling postdoctoral research fellowship programmes. If any of the projects below pique your interest, please reach out! I am passionate to get this study system running at full speed, and interested researchers are more than welcome on board. Using CRISPR to develop novel genetic tools in Drosophila testaceaSuitable for Masters, PhD, or Postdoctoral researchers
 A short but sweet post: join us!
I have a funded PhD studentship opportunity to for 3.5 years to characterise aphid immune evolution. Details can be found at the link below: www.exeter.ac.uk/study/funding/award/?id=5191 The project is co-supervised by myelf (lead supervisor), Bartek Troczka, and Chris Bass. Feel free to drop me an email at [email protected] for more information. You can also use the Contact form on the website here. Cheers, Mark |
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