The dynamic interplay between virulence factors of a pathogen and the immune system of a host determines whether disease will occur. A deep understanding of the molecular mechanisms that underlie host-pathogen arms race is essential for developing durable resistance. Pathogens have evolved a large and diverse complement of virulence proteins, called effectors, which, collectively, are indispensable for disease development. An important feature of effectors is their fast evolution driven by adaptation towards a host.

Confined epidermal cells mimic in vivo migration and reveal volume-speed relationship
By: Ellie Labuz (Theriot Lab)

Functional Evolution of a Meristem Identity Gene
By: Hannah McConnell (Di Stilio Lab)

In bacteria, plasmids can move horizontally between cells of the same and different species through the process of conjugation. When a plasmid imposes a fitness cost on its bacterial host, a sufficiently high level of conjugation is required to maintain the extrachromosomal element in the population (effectively as a molecular parasite). For costly plasmids with low conjugation rates, their long-term persistence presents a paradox. Prime examples of this paradoxical persistence concern plasmids that house antibiotic resistance genes, which can be costly in the absence of antibiotics.