Education & Training
- B.A. Biology and Biochemistry, Oberlin College, 2007
- Ph.D. Molecular and Cell Biology, UC Berkeley, 2014
Research Interest Summary
The Levin lab started in July 2020 in the Biological Sciences department at Pitt. Our work focuses on the evolution of infectious diseases, seeking to understand how evolutionary “arms races” between hosts and pathogens dynamically shape the biology of immunity and pathogenesis. We approach these questions using a combination of high-throughput genetics, microbiology, and evolutionary genomics, focusing on the opportunistic pathogen Legionella pneumophila and its natural hosts, environmental amoebae.
Many opportunistic pathogens spend much of their time outside of a human host, living instead in water or soil environments. What natural pressures select for bacterial virulence in the wild? One major, under-appreciated force is the need for bacteria to fight off predators, particularly eukaryotes that eat bacteria, such as amoebae. In fact, many bacterial pathogens use the same molecular machinery to attack and infect amoebae as they use to combat our own cells during human infections. This suggests that amoebae serve as “evolutionary training grounds”, selecting for microbes that can subvert eukaryotic defenses. My lab studies how amoebae and bacterial pathogens co-evolve, with the idea that these dynamics can transform innocuous environmental bacteria into novel human (and amoeba) pathogens. This has certainly been the case for the bacterium Legionella pneumophila, which has evolved to cause a deadly, pneumonia-like disease in humans via adaptation to its natural, amoeba hosts. My lab leverages the highly tractable Legionella bacteria/Dictyostelium amoeba system to deduce how this “evolutionary training” occurs.
Our current projects include those on both the host and microbe side. These include: 1) comparative genomic approaches to find evolutionary signatures of arms races, 2) high-throughput screens to discover the genes most functionally relevant during infections, and 3) candidate gene approaches to determine how adaptation has changed host-microbe molecular interactions.
Richter DJ, Levin TC. (2019) The origin and evolution of cell-intrinsic antibacterial defenses in eukaryotes. Current Opinion in Genetics & Development 58:111-122.
Levin TC, Goldspiel BP, Malik, HS. (2019) Density-dependent resistance protects Legionella pneumophila from its own antimicrobial metabolite, HGA. eLife 8:e46086. eLife digest about this paper
Levin TC and Malik, HS. (2017) Rapidly evolving Toll-3/4 genes encode male-specific Toll-like receptors in Drosophila. Molecular Biology and Evolution 34(9): 2307-2323.