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R L Russell

Publications and source records attributed to R L Russell.

107 records · Page 6Linked to original sources
PubMed1974

Comparative genetics of the T-even bacteriophages.

A system of amber mutants has been developed for each of the T-even bacteriophages T2 and T6, to complement those already available in T4. In T2 these mutants identify 52 genes, of which 49 are homologous with T4 genes; in T6 they identify 45 genes, of which 42 have T4 homologs, and an additional one which is homologous to a T2 gene not yet identified in T4. In both T2 and T6, recombination between mutants is characterized by considerable negative interference, which is correctable by a mapping function designed for T4. Recombinational maps of T2 and T6 constructed with these mutants have the same gene order and nearly the same gene spacings as in T4, with the exception of the tail fiber region; T2 and T6 appear to lack a localized recombinational expansion of this region found in T4. Homologous gene products from all three phages are in general interchangeable, with the exception of those from two apparently "co-adapted" tail fiber genes, 37 and 38. The general genetic similarity of all three phages suggests that they are analogous to races of higher organisms, retaining the capacity for genetic exchange despite some clear genetic differences and some incipient isolating mechanisms.

Chromosome Mapping↗
PubMed1974

Partial exclusion between T-even bacteriophages: an incipient genetic isolation mechanism.

Conditional lethal mutant systems developed in T-even bacteriophages T2, T4 and T6 have been used to study the partial exclusion which characterizes mixed infections of these phages. In bacteria mixedly infected with T2 and T4, the dominant phage (T4) acts against localized exclusion sensitivity determinants in the genome of the excluded phage (T2). These determinants are clustered near genes controlling early functions; the determinants themselves do not appear among the progeny, but markers located close to them appear infrequently, by recombination. The excluding action of T4 does not depend on the action of any gene so far identified by conditional lethal mutations, nor does it depend on differences in DNA glucosylation between infecting phages. Regardless of mechanism, the genetic consequence of this partial exclusion is to limit genetic exchange between T2 and T4 in the region of the genome controlling early functions, while retaining the capacity for extensive exchange in other regions; in short, partial exclusion constitutes a localized genetic isolating mechanism. Related forms of partial exclusion characterize mixed infections of other T-even phages, including those of some phages newly isolated from nature.

Chromosome Mapping↗
PubMedDate not supplied

Quantitative measures of aging in the nematode Caenorhabditis elegans: II. Lysosomal hydrolases as markers of senescence.

In an attempt to provide additional quantitative markers of senescence in the nematode Caenorhabditis elegans, we have identified age-dependent increases in four lysosomal enzymes: acid phosphatase, beta-N-acetyl-D-glucosaminidase, beta-D-glucosidase, and alpha-D-mannosidase. These enzymes were judged to be lysosomal on the basis of their resemblance to analogous mammalian lysosomal enzymes with regard to subcellular fractionation, lectin binding, Km, molecular weights, inhibitor sensitivities, and pH optima. In nematode populations which had a median lifespan of 8.9 +/- 0.7 days and a maximum lifespan of 14-16 days, we observed the following increases in acid hydrolase activities per animal from day 3 (early adulthood) to day 10: (1) up to 2.5-fold for acid phosphatase; (2) 8-fold for beta-N-acetyl-D-glucosaminidase; (3) 9-fold for beta-D-glucosidase; and (4) 4-fold for alpha-D-mannosidase. Three forms of acid phosphatase and two forms of beta-D-glucosidase were separated by ion-exchange chromatography, but in each case only one form of the enzyme was primarily responsible for the age-dependent increase in total activity: acid phosphatase I increased 18-fold, while beta-D-glucosidase I increased 100-fold. By contrast, there were only slight age-dependent changes in choline acetyltransferase, acetylcholinesterase, or alpha-D-glucosidase activities after early adulthood. The age-dependent increases in acid phosphatase, beta-N-acetyl-D-glucosaminidase, beta-D-glucosidase, and alpha-D-mannosidase activities are sufficiently large and reproducible to be useful quantitative markers of senescence in C. elegans.

Acetylglucosaminidase↗