Bacterial populations are often clonal, and even within a bacterial species, the frequency of gene exchange and recombination is quite low. Consequently, mobile genetic elements--plasmids, bacteriophages, and transposons--have been the central factors in the evolution of pathogenic traits. One central feature of pathogenicity, the capacity to enter epithelial cells, is encoded by the bacterial chromosome of Yersinia pseudotuberculosis but by plasmid genes in enteroinvasive Escherichia coli. A single Yersinia gene, inv, which encodes a single 107,000-dalton protein, can be cloned in E. coli K12, and its presence is sufficient to permit the bacteria to enter cultured human cells. In contrast, fully 70 kilobases of a virulence plasmid from enteroinvasive E. coli must be transferred to E. coli K12 to achieve the same result. While researchers are at the early stages of understanding microbial entry into host cells, they can now investigate the molecular basis of this event in greater detail than has previously been possible.