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Biomedical subjects

A Campbell

Publications and source records attributed to A Campbell.

At least 289 records · Page 16Linked to original sources
PubMed1972

A mutant of Escherichia coli that requires high concentrations of biotin.

A recessive mutation (bir) of E. coli, at 77 min on the standard map, destroys ability of the bacteria to take up biotin or to grow except at high concentrations of biotin. In a biotin prototroph, the bir mutation causes overproduction and excretion of biotin, and derepression of at least one biosynthetic gene (bioD). Growth of the bir mutant is inhibited by avidin or high concentrations of dethiobiotin. Both effects are reversed by biotin.

Biotin↗
PubMed1972

Location of promoter and operator sites in the biotin gene cluster of Escherichia coli.

Biotin independence in E. coli requires five closely linked genes, bioA, bioB, bioF, bioC, and bioD. The residual gene activity of deletion mutants has been studied by complementation and enzyme assays. Deletion of the left end of the bioA gene does not impair expression of the remaining genes, but deletions from the left extending into bioB abolish all gene expression. Nonsense mutations in bioB reduce expression of bioC, bioF, and bioD. Therefore, the four genes, bioB, bioF, bioC, and bioD, are transcribed as a unit from left to right, from a promotor located between bioA and bioB. Expression of the bio genes is repressible by added biotin. Deletions removing the left end of bioA do not affect repressibility of bioD. Therefore the operator, as well as the promoter, lie to the right of bioA. One deletion that removes bioA, bioB, and bioF renders the bioD gene constitutive, presumably by fusion to an unknown operon. Therefore, the operator lies to the left of bioC.

Biotin↗
PubMed1972

Deletion and complementation analysis of biotin gene cluster of Escherichia coli.

Genetic deletions that terminate within the cluster of genes needed for biotin biosynthesis in Escherichia coli have been isolated and mapped by transduction with phages lambda and P1. These deletions order the point mutations in each of the five genes. Mutations causing biotin dependence were incorporated into lambdapbio transducing phages. New bio(-) mutations were induced by exposure of lambdapbio particles to ultraviolet light. Tests of complementation between such bio(-)pbio particles and bio(-) mutant cells divide the bio(-) mutations into five cistrons: bioA, bioB, bioF, bioC, and bioD. Certain bioA and bioF mutations exhibit intragenic complementation, suggesting that these genes determine enzymes composed of identical subunits.

Biotin↗
PubMed1972

Gene regulation in N mutants of bacteriophage lambda.

Mutants (N(-)nin) of bacteriophage lambda in which the N gene product is not required for growth on wild-type Escherichia coli do not plate on recA bacterial mutants. Secondary mutants, selected for growth on recA, lie within the immunity region to the right of gene cI and appear identical to the cro mutants of Eisen et al. In an N(+) phage, a cro mutation causes enhanced and prolonged production of lambda exonuclease. N(-)cro phages make no detectable exonuclease, but show an increased rate of specific excision from lysogens and are excluded by P2 prophage. These properties, together with the ability to plate on recA, suggest that N(-)cro phages express genes to the left of N at a rate that is very low but higher than that for N(-)cro(+) phages. N(-)nin phages can integrate at the normal site on the bacterial chromosome, but specific excision from lysogens is immeasurably low.

Binding Sites↗