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A method is described for estimating quantitatively the frequency of transformation of pneumococci to new capsular types. It is found that, when S-(III) cells are exposed to deoxyribonucleic acid (DNA) from wild-type I strains, transformation to SI occurs at a frequency 20 to 60 times that of transformation to the binary type SI-III. SI markers on DNA isolated from binary strains behave qualitatively and quantitatively in a different manner from the same markers on DNA from wild-type I strains and will transform S-(III) cells only to SI-III. Strains are described which produce only one capsular polysaccharide, but which are genetically binary and carry a second capsular genome with a mutated gene so that the second polysaccharide is not produced. Stability and other characteristics of binary strains are discussed, and one hypothesis for the genetic organization of binary strains is presented.

The genetic behavior in transformation reactions of 20 noncapsulated mutants of pneumococcus type III suggests that each has a single-site mutation in the locus controlling the synthesis of uridine diphosphate glucose (UDPG) dehydrogenase. Each strain is capable of yielding transformants of the binary capsular type SI-III when exposed to deoxyribonucleic acid (DNA) from type I cells. One additional mutant reacted differently and behaved as if it were a multisite mutant with the mutation affecting both the locus for UDPG dehydrogenase and that controlling the synthesis of high molecular weight type III capsular polysaccharide. When exposed to DNA from type I pneumococci, this strain yielded transformants which were genotypically binary but which expressed only the type I capsular phenotype.

Through transformation reactions, binary capsulated SI-III strains of pneumococci have been isolated that are unstable and lose the SI capsular genome at high frequency. The instability is caused by the specific mutation in the SIII capsular genome common to all of the unstable strains. In the family of strains studied, the SI capsular genome was integrated into the recipient chromosome in at least two loci: one apparently adjacent to the resident capsular genome and a second some distance from it. A hypothesis is presented to explain the instability of the strains on the basis of redundancy of genetic information.