I am a Swiss NSF Mobility Research Fellow at the University of Exeter.
Google Scholar / Personal Webpage / Twitter: @HansonM90 / Mastodon: @MarkHanson@drosophila.social,
|2022-||SNF Mobility Research Fellow|
|2017-2021||EPFL Switzerland||PhD with Bruno Lemaitre|
|2008-2017||University of Victoria||BSc followed by MSc with Steve Perlman then research assistant|
I am interested in how the immune system evolves to defend against different pathogens. This blossomed in my Masters degree with Steve Perlman at the University of Victoria. My thesis work in Bruno Lemaitre’s lab at EPFL Switzerland overturned a decades-old paradigm on the role of “antimicrobial peptides” in defence. Antimicrobial peptides are exactly what they sound like: they’re host-encoded antibiotic genes. These immune effectors are regulated by core signalling pathways common to all animals. This was only made possible with the advent of CRISPR gene editing and the power of Drosophila genetics. We made flies carrying mutations for 14 genes from seven gene families, both individually and all combined together. With those flies, the first animal model lacking most of its antimicrobial peptide genes, we could test the importance of AMPs in live animals from a genetic perspective. That overturned a lot of the assumptions of the field, as we realised the many, many AMPs produced by organisms weren’t just this generalist antibiotic cocktail, but rather, we found evidence that individual genes were tailored to fight specific pathogens.
For my post-doctoral work, I’m taking a step back. We regularly assume that conservation of immune pathway genes equals conservation of the flow of information from the top to the bottom of those signalling pathways. Basically, if all the same genes are there, we assume that the hierarchy and signalling structure is also the same. My work in the Longdon lab is going to test that assumption. Stay tuned to my Twitter, Mastodon, or Google Scholar profile to see up-to-date work!