摘要：

The colicinogenic plasmid Col V-K94 and the class of transferable drug-resistance factors that inhibit fertility of the sex factor, F, are believed to be genetically similar to F. Heteroduplexes between these various F-like plasmids were studied by electron microscopy in order to identify and define the DNA segments that contain genes coding for fertility and other common functions. It was found that approximately 44% of the F factor is homologous to several different fi + R factors and to Col V-K94, and that all of the homology between these plasmids and F is restricted to a region comprising only one-half of the F-factor molecule. These data, and previously reported electron microscope mapping of deletions of F factors, suggest that the genes active in the process of transfer are contained in one-half of the F factor, and therefore imply that the other half of F might not be required for expression of its fertility functions. DNA sequence homology among the R factors R6, R100 and R1 was also studied by heteroduplex formation. All of the DNA sequences contained in R100 were observed to be present in R6, and approximately 85% of the DNA sequences of R1 were included in R6. In the R1 R6 heteroduplex, homology is distributed equally in the R-factor region homologous to the F factor, and the region containing antibiotic-resistance determinants (i.e. the segment deleted in the resistance transfer factor unit, RTF). The position of certain drugresistance determinants has been mapped by using various R-factor deletion mutants and correlating the pattern of drug resistance with the sequence homology observed among different R factors. Unlike the other resistance-determinant genes identified, the tetracycline marker has been mapped in the segment of R6 that is largely homologous to the F factor. Inverted repeats, which consist of DNA segments repeated in reverse sequence on the same single strand of DNA, were observed in R6, R100 and Col V-K94. One inverted repeat of R6 is located near the tetraeycline marker. Further duplication of one of the complementary sequences of the inverted repeat, and insertion of this duplication into the plasmid genome apparently inactivates the tetracycline-resistance determinant of R6.

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