Abstract
An Escherichia coli-Shigella flexneri hybrid of intermediate virulence was studied to determine whether its shorter survival in host cells might be due to a metabolic defect. Investigation of its growth in minimal glucose medium showed that the hybrid, like its E. coli parent, had a longer lag phase and a slower growth rate than its virulent Shigella parent. Methionine was found to increase the growth rate of the hybrid. The Shigella parent of the hybrid can synthesize methionine normally, but the E. coli parent has a point mutation in its metA gene. Since it synthesizes enough methionine to grow slowly, it is postulated that the hybrid strain has a hybrid metA gene, that is, a gene composed partly of deoxyribonucleic acid (DNA) from E. coli, with the balance of the DNA from S. flexneri. Phage P1-mediated transduction, with the metA(-)E. coli parent as recipient and the Shigella parent as donor, yielded a few transductants that responded to methionine in the same way the hybrid did. Many more transductants of the hybrid type were produced when the hybrid strain was used as a donor. It is suggested that this poorly functioning gene acts synergistically with the hybrid strain's relaxed synthesis of ribonucleic acid to prevent its survival in the host.