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Biomedical subjects

J Felton

Publications and source records attributed to J Felton.

8 recordsLinked to original sources
PubMed1988

Implantation of Bacteroides gingivalis in nonhuman primates initiates progression of periodontitis.

Although periodontitis is a bacterial disease, its multidimensional nature and its bacterial complexity have made it difficult to definitively prove that specific microorganisms initiate the disease process. The successful implantation of a rifampin-resistant strain of the putative periodontal pathogen Bacteroides gingivalis into the periodontal microbiota of monkeys (Macaca fascicularis) resulted in an increase in the systemic levels of antibody to the microorganism and rapid and significant bone loss.

Animals↗
PubMed1980

Mutations in two unlinked genes are required to produce asparagine auxotrophy in Escherichia coli.

Escherichia coli K-12 has two genes, asnA+ and asnB+, either one of which is able to satisfy the need of cells for asparagine. In order for a strain to have an auxotrophic requirement for asparagine, both genes must be mutationally inactivated. We obtained mutants with Tn5 inserted in asnB. asnB was mapped by conjugation and by three-factor P1 transductions at 15 min on the E coli K-12 linkage map, between ubiF and nagB. Specialized transducing phage lamba 781 supE was shown to carry asnB, as well as supE, ubiF, nagA, and nagB. asnA is the previously mapped ilv-linked asn locus, whiich is between uncB and rbs. E. coli C also has two asn genes, corresponding to asnA and asnB.

Aspartate-Ammonia Ligase↗
PubMed1979

Plasmid pSC101 replication in integratively suppressed cells requires dnaA function.

Maintenance of plasmid pKC17, a derivative of plasmid pSC101, in E. coli requires a functional dnaA gene product. This was demonstrated by segregation experiments using an E. coli dnaA46 mutant, at various temperatures. Growth of this mutant at elevated temperature was allowed by the presence of a P2sig5 prophage. rpoB mutations, which suppress the temperature sensitivity of a dnaA46 mutant permit efficient maintenance of plasmid pKC17 at temperatures up to 40 degrees, conditions which normally inactivate the dnaA46 product.

DNA Replication↗
PubMed1976

Genetic determination of the beta-galactosidase developmental program in mouse liver.

The developmental program for beta-galactosidase in C57BL/6J and related strains of mice differs from that seen in most other mouse strains. Mice of the C57BL/6 group show a rise in liver enzyme activity during development that is not seen in mice of other strains. The developmental pattern of beta-galactosidase activity in heart and brain of C57BL/6 mice is similar to that in other strains. Physical, kinetic, and immunological tests indicate that the developmental increase in C57BL/6 enzyme activity is an increase in the number of molecules of the same species of enzyme protein that is present in other strains. In genetic crosses, the presence of the developmental rise in liver enzyme activity segregates as if determined by a single genetic factor showing additive expression in heterozygotes. This factor is closely linked to the beta-galactosidase structural gene on chromosome 9. The existence of a genetic variant with these properties is evidence that programmatic information capable of regulating the temporal expression of a structural gene can be encoded in DNA.

Animals↗