THE MECHANISMS OF TRANSFER OF R FACTORS

抄録

Kinetic studies of transfer of R and F factors showed that transfer events distribute with a single-peaked homologous pattern in established (normal state) R factor as well as its HFRT systems and F' factor. These results indicate that the differences of transmission frequencies in these states are due to the differ-ences in the number of transmissible competent cells in the donor populations. The transfer of these episomes requires cell-to-cell contact between donor and reci-pient bacteria. The frequencies of formation of specific cell pairing counted under a phase contrast microscope were in good accordance with the frequencies of transfer of these episomes, and inhibiting agents of this cellular union dis-closed some physiological properties of the organelle which takes part in cell-to-cell contact.
Electronmicroscopic observation of the donor cells demonstrated the presence of specific pili on their surface. The frequencies of cells having specific pili counted by electronmicroscopy and the frequencies of phase f2-sensitive bac-teria in donor cultures carrying various episomes were in good accordance with the frequencies of their transfer. Furthermore, the physiological properties specific for donor bacteria seem to. be easily explained by the presence of spe-cific pili on their surface. All of these findings suggest that these specific pili may be organelles for forming conjugation bridges for the transfer of episomes.
Analysis of superinfection immunities of R and F factors indicated that the greater part of the inhibition of acceptance of superinfecting non-viral episomes is due to the inhibition of acceptance on the surface of recipient cells which already have homologous episomes and that mutual exclusion between homologous episomes in the same cell is also involved. These results suggest the presence of specific receptors on the cell surface and of specific sites for their replications inside the cell. The sites for replication may be different among F, ƒi⁺ R and fi^- R factors, and may be present in small numbers assuming from the data of superinfection immunities. Specific pilus for each episome is probably formed immediately outside of this specific site in view of the rapid transfer of episomes.
Acriflavine, an inhibitor of DNA synthesis, was shown to inhibit the trans-fer of episomes but not to inhibit specific cell pairing and evidence was obtained that this inhibition occurs in donor bacteria. These results suggest that the transfer of episomes may require specific DNA replication for their transfer.
The phenotypic expression of drug resistances was found to require spe-cific protein synthesis, because the expression of drug resistances is suppressed by inhibitors of protein synthesis.