Speaker
Description
Plasmids are mobile genetic elements that horizontally transfer antibiotic resistance and virulence factor genes among bacteria. It's unclear if plasmids persist only through selection for the genes they carry or if they are infectious enough to persist as genomic parasites. Here we show that plasmids' infectious potential is severely underestimated by theoretical models and experimental assays that overlook the epidemiological consequences of self-repressed transfer. Many plasmids express transfer genes in newly-infected cells but later repress them, a phenomenon known as transitory derepression or fertility inhibition. We experimentally measure the epidemiological dynamics of IncF plasmids in E. coli and show that self-repression delays infectious spread but does not slow it. Plasmid infectiousness persists through stationary phase but declines rapidly when cultured without new susceptible cells. Self-repression lets plasmids stochastically adjust their investment in horizontal transmission, reducing the net fitness cost of expressing transfer genes while still allowing epidemic spread in susceptible cell populations. These results show how plasmid epidemiology differs from the idealized agents of current models and reveal an underestimated ability to spread without direct selection for plasmid-borne genes.
