On the specificity of the desoxyribonucleic acid which induces streptomycin resistance in Hemophilus.

Streptomycin resistance of a high degree has been induced in sensitive populations of Hemophilus influenzae and Hemophilus parainfluenzae by desoxyribonucleic acids (DNA's) derived from streptomycin (SM)-resistant cells of at least one heterologous species of Hemophilus. The specificity of the DNA which controls SM resistance has been studied within and among species of Hemophilus by comparing, in a given population, the proportion of cells transformed to SM-resistant by DNA's derived from highly resistant cells of heterologous type or species with the proportion changed by the DNA derived from SM-resistant cells of the homologous type or species. The ratio resulting from this comparison correlates in general with the degree of kinship between recipient and donor cells suggested by accepted methods of bacteriologic classification. The numerical value of the ratio is much lower when the species of the recipient population and donor of the DNA differ than when they are of the same species. The data suggest that this ratio is of value as an index of degree of kinship of recipient and donor cells. Comparison of the activity of heterologous and homologous DNA's shows differences within species and degrees of differences among species not brought out by other available methods. The data suggest that H. influenzae is more closely related to H. parainfluenzae than to H. suis and that the relationship between H. parainfluenzae and H. suis is remote. Within the species H. influenzae and H. parainfluenzae the ratio of hetero-specific transformants to homospecific transformants appears to be relatively constant for a given recipient population. This ratio also appears to be independent of the type or group source of the heterologous species SM resistance DNA. The low proportion of cells in H. influenzae populations which are transformed to SM-resistant by DNA's derived from SM-resistant H. parainfluenzae and vice versa has been increased 4- to 15-fold by the replication of the heterologous species SM resistance DNA in the heterologous species. An alteration of the heterologous DNA by the host is suggested.