Drosophila infected by green fluorescent bacteria.
Red-eyed flies lacking antimicrobial peptides are
susceptible to infection, while white-eyed flies with
antimicrobial peptides resist infection.
At the interface of host-pathogen interactions
I study the evolution of the immune system. Because surviving infections is so important, our immune system is adapted to fight many parasites and pathogens. My research focuses on immune effectors, i.e. the things that directly kills germs. I've found that these effectors aren't always just generic "kill-everything" genes, but some of them are actually targeted silver bullets that fight specific germs we are commonly exposed to. It's a profound realisation that our genes, our genome, is shaped so strongly by specific germs in such tailored fashions.
In my ongoing work, I am taking a step back to ask how these geners are regulated across species. A basic assumption we all make about how immunity "works" is that specific genes do specific things. There are also these "pathways" that get activated, leading to inflammation. Now that sequencing genomes is so easy, we're doing it a lot, and using those genomes to try to predict things like "why is species X susceptible to SARS-CoV-2, but not species Y?"** But one of the basic assumptions we make is that if all the same genes are present across species, the pathways transmit information in the same way. That's a reasonable assumption, but I'm not so sure it's true... at least not universally. Using Drosophila genetics and an evolutionary approach, I will test just how common it is that "all the same genes are present" means "the pathways are the same" across species.
I study the evolution of the immune system. Because surviving infections is so important, our immune system is adapted to fight many parasites and pathogens. My research focuses on immune effectors, i.e. the things that directly kills germs. I've found that these effectors aren't always just generic "kill-everything" genes, but some of them are actually targeted silver bullets that fight specific germs we are commonly exposed to. It's a profound realisation that our genes, our genome, is shaped so strongly by specific germs in such tailored fashions.
In my ongoing work, I am taking a step back to ask how these geners are regulated across species. A basic assumption we all make about how immunity "works" is that specific genes do specific things. There are also these "pathways" that get activated, leading to inflammation. Now that sequencing genomes is so easy, we're doing it a lot, and using those genomes to try to predict things like "why is species X susceptible to SARS-CoV-2, but not species Y?"** But one of the basic assumptions we make is that if all the same genes are present across species, the pathways transmit information in the same way. That's a reasonable assumption, but I'm not so sure it's true... at least not universally. Using Drosophila genetics and an evolutionary approach, I will test just how common it is that "all the same genes are present" means "the pathways are the same" across species.
"Time flies like an arrow, fruit flies like a banana." My research has shown that not only do flies like a banana, but the banana presents a niche filled with certain bacteria, and those bacteria impose selection on the fly immune system in highly specific ways. This pattern holds for flies with different ecologies, like mushroom-feeders or plant parasites.
Article synopsis here: https://www.science.org/doi/10.1126/science.adg5725
Full text (free) here: https://mahansonresearch.weebly.com/uploads/1/2/3/6/123603726/hanson_science.adg5725.pdf
Art by https://sci-flies.com/
Why fruit flies?
Drosophila fruit flies are a great model for my work since they are easy to rear, grow quick, cheap to care for, and have the same sorts of immune response genes as humans (e.g. "Toll-like receptors"). It also helps that I don't feel personally too too bad about stabbing a fruit fly with a bacteria-laced needle. I'd have to juggle far more ethical implications to carry out my work on another animal model like lab mice. Not only that, the Drosophila immune response is both simpler than humans or mice, and incredibly well-studied. That means it's easy to observe something new and then understand what it means in a broader context. But I should say that fly research also directly translates to other animals, including economically-important insects and arthropods, like the terrifying, jigsaw-wielding Spotted-wing Drosophila "Drosophila suzukii" (OoooOooh...).
**Note: There are other important cross-species pathogens from SARS2, but hey, everyone knows SARS2 nowadays. It's a good example.
Drosophila fruit flies are a great model for my work since they are easy to rear, grow quick, cheap to care for, and have the same sorts of immune response genes as humans (e.g. "Toll-like receptors"). It also helps that I don't feel personally too too bad about stabbing a fruit fly with a bacteria-laced needle. I'd have to juggle far more ethical implications to carry out my work on another animal model like lab mice. Not only that, the Drosophila immune response is both simpler than humans or mice, and incredibly well-studied. That means it's easy to observe something new and then understand what it means in a broader context. But I should say that fly research also directly translates to other animals, including economically-important insects and arthropods, like the terrifying, jigsaw-wielding Spotted-wing Drosophila "Drosophila suzukii" (OoooOooh...).
**Note: There are other important cross-species pathogens from SARS2, but hey, everyone knows SARS2 nowadays. It's a good example.
This is Mark A. Hanson's research page. I did my PhD in Dr. Bruno Lemaitre's lab at l'École Polytechnique Fédérale de Lausanne (EPFL), in Lausanne Switzerland. After this I spent some time as a post-doc and research associate in the Lemaitre lab and Dr. Ben Longdon's lab at the University of Exeter, Penryn, UK funded by the Swiss National Science Foundation (SNSF). Starting in late 2023, I will be a Wellcome Trust ECA fellow working with Dr. Longdon to better understand the evolution of host immune signalling. The Longdon lab investigates how infection dynamics differ across species, with a previous focus on viruses. My work will characterize how immune signalling differences evolve across species. This collaboration will help study the what, why, and how of differences in immune competence across species. That question is particularly relevant in the post-pandemic era, where animal spillovers are a threat to global health.
