University of Utah
Talia Karasov Lab
Talia Karasov is an assistant professor in the School of Biological Sciences at the University of Utah. A central goal of my lab is to understand how bacterial pathogens evolve to colonize different host species and how hosts evolve resistance. Focusing on the bacterial genus Pseudomonas and its plant and animal hosts, our work combines comparative genomics, genetic analysis and metabolomics to determine the molecular basis of pathogen strain preferences. Recently we discovered that a phage-derived tailocin may be a major determinant of pathogen success in Pseudomonas host populations. We are currently studying the coevolution of tailocin tail fibers and the surrounding competing bacteria.
Affiliations: (1). School of Biological Sciences, University of Utah, Salt Lake City, UT 84112 (USA) (2). Centre for Life’s Origins and Evolution, Department of Genetics, Evolution and Environment, University College London, London (UK)
Pseudomonas plant pathogens encode a conserved mechanism of competition — a phage-derived element termed a tailocin, which they use to kill competitors. With a mechanism of action similar to phage, the tailocin tail fibers encode specificity and target subsets of co-occurring pathogenic strains. Surprisingly, the most lethal tailocin variants are at low frequencies in the pathogen populations and have not outcompeted their neighbors. This finding suggests the presence of a trade-off between broad-spectrum killing and an unknown pathogen fitness trait. Here we investigate constraints on the evolution of the tail fibers and killing spectrum. We find that the most lethal tailocins are associated with LPS variants that compromise Pseudomonas survival in the host. The pathogens have evolved a limited repertoire of tail fibers and LPS variants in part due to this trade-off, suggesting strong constraints on the evolution of new tail fiber and LPS variation