Ralstonia eutropha JMP134 (pJP4) is a useful model for the study of bacterial degradation of substituted aromatic pollutants. Several key degrading capabilities, encoded by tfd genes, are located in the 88 kb, self-transmissible, IncP-1 beta plasmid pJP4. The complete sequence of the 87,688 nucleotides of pJP4, encoding 83 open reading frames (ORFs), is reported. Most of the coding sequence corresponds to a well-conserved IncP-1 beta backbone and the previously reported tfd genes. In addition, we found hypothetical proteins putatively involved in the transport of aromatic compounds and short-chain fatty acid oxidation. ORFs related to mobile elements, including the Tn501-encoded mercury resistance determinants, an IS1071-based composite transposon and a cryptic class II transposon, are also present in pJP4. These mobile elements are inefficient in transposition and are located in two regions of pJP4 that are rich in remnants of lateral gene transfer events. pJP4 plasmid was able to capture chromosomal genes and form hybrid plasmids with the IncP-1 alpha plasmid RP4. These observations are integrated into a model for the evolution of pJP4, which reveals mechanisms of bacterial adaptation to degrade pollutants.

In this study population (105 schoolchildren aged 5.5-11.5 yrs), dental decay was detected in 75.2% and S. mutans in 55.2% of the subjects. The presence of S. mutans was assessed - using the selective GSTB medium - in unstimulated saliva and in pooled occlusal and pooled buccal plaques from the four most posterior teeth. All three samples showed association between S. mutans presence and caries prevalence. Of the two types of plaque, the occlusal not only had a higher frequency of isolation but also a significantly higher proportion of S. mutans. The presence of S. mutans was significantly associated with both caries prevalence and extent of caries experience. Both S. mutans prevalence and S. mutans proportion in plaque increased with the number of decayed teeth present among those sampled. Sucrose consumption between meals appeared to be more correlated with the degree of caries experience rather than with caries or S. mutans prevalence. A second clinical examination was scheduled six months after the first for S. mutans-positive children who either were free of active carious lesions, or were caries-active but without signs of dental decay in the sampled teeth. Caries-active subjects proved to be more prone to new carious lesions than caries-free subjects, who tended to remain caries-free even when they had a high proportion of S. mutans in plaque, thus indicating the basic importance of the host factor in the caries process.

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When an R determinant for streptomycin is transferred into a conditionally streptomycin-dependent E. coli B mutant—which requires in minimal medium either histidine or streptomycin—the latter behaves like a histidineless strain. This phenotype modification shows that the repairing action of streptomycin is prevented. The specific requirement of the strain is not now replaced even by streptomycin concentrations up to 10000 µg/ml at which the conditionally streptomycin-dependent mutant could originally grow, and which are well beyond the resistance level characteristic of the R determinant itself. These data seem to suggest that a reduction in permeability of the cell membrane cannot be held responsible for the phenomenon observed.