Selection for phenotypic plasticity in Rana sylvatica tadpoles

The hypothesis that phenotypic plasticity is an adaptation to environmental variation rests on the two assumptions that plasticity improves the performance of individuals that possess it, and that it evolved in response to selection imposed in heterogeneous environments. The first assumption has been upheld by studies showing the beneficial nature of plasticity. The second assumption is difficult to test since it requires knowing about selection acting in the past. However, it can be tested in its general form by asking whether natural selection currently acts to maintain phenotypic plasticity. We adopted this approach in a study of plastic morphological traits in larvae of the wood frog, Rana sybatica. First we reared tadpoles in artificial ponds for 18 days, in either the presence or absence of Anax dragonfly larvae (confined within cages to prevent them from killing the tadpoles). These conditioning treatments produced dramatic differences in size and shape: tadpoles from ponds with predators were smaller and had relatively short bodies and deep tail fins. We estimated selection by Anax on the two kinds of tadpoles by testing for non-random mortality in overnight predation trials. Dragonflies imposed strong selection by preferentially killing individuals with relatively shallow and short tail fins, and narrow tail muscles. The same traits that exhibited the strongest plasticity were under the strongest selection, except that tail muscle width exhibited no plasticity but experienced strong increasing selection. A laboratory competition experiment, testing for selection in the absence of predators, showed that tadpoles with deep tail fins grew relatively slowly. In the cattle tanks, where there were also no free predators, the predator-induced phenotype survived more poorly and developed slowly, but this cost was apparently not associated with particular morphological traits. These results indicate that selection is currently promoting morphological plasticity in R. sylvatica, and support the hypothesis that plasticity represents an adaptation to variable predator environments.     

Cycling, stressed-out and nervous: cellular functions of c-Abl.

c-Abl, the product of the cellular homologue of the transforming gene of Abelson murine leukaemia virus, has been a protein in search of a purpose for over two decades. Because c-Abl is implicated in the pathogenesis of several human leukaemias, understanding the functions of Abl is an important goal. Recently, biochemical and genetic approaches have converged to shed new light on the mechanism of regulation of c-Abl kinase activity and the multiple roles of c-Abl in cellular physiology. This review summarizes our current understanding of the many facets of c-Abl biology, emphasizing recent studies on Drosophila and mammalian Abl.     

A quantitative histochemical study of NADPH-ferrihemoprotein reductase activity

Summary A quantitative histochemical assay for NADPH-ferrihemoprotein (P450) reductase had been developed. For optimal activity, it is necessary to use a relatively electropositive tetrazolium salt such as neotetrazolium chloride as the final acceptor. The apparentK _m of the reaction is 0.83 mM. Its specificity has been proven in two ways: (i) activity is increased selectively in the pericentral zone of liver from rats treated with phenobarbitone, an inducer of the reductase, though not in liver of rats injected with 3-methylcholanthrene, which induces NAD(P)H dehydrogenase; (ii) it is competitively inhibited by NADP⁺ (K _i=1.50mm) though unaffected by dicumarol, an inhibitor of NAD(P)H dehydrogenase activity. An NADP⁺ concentration ten times greater than the substrate concentration inhibits the histochemical reaction and the reaction in a microsomal fraction assayed biochemically to the same degree (70% inhibition). The amount of inhibition is independent of temperature, of the zone of the acinus and of the treatment of the animal.Continuous microdensitometric monitoring of the reaction product as it is formed has shown that the specific reaction is linear with incubation up to 10 min, thus allowing end-point measurements to be used for cytophotometric analysis.     

Calcium-stimulated myofibrillar ATPase activity correlates with shortening velocity of muscle fibres in Xenopus laevis

Summary The iliofibularis muscle ofXenopus laevis is reported to contain five types of fibres which have different force—velocity relationships. Ten fibres of each type were selected on the basis of succinate dehydrogenase activity, cross-sectional area and location in the muscle, in order to assess the validity of the fibre type classification.Maximum calcium-stimulated myofibrillar ATPase activity (V _max) and apparent Michaelis constant (K _m) for ATP were determined for these 50 fibres from serial sections. The values obtained varied according to the type of fibre. Type 1 had the highest and type 5 the lowest values forK _m andV _max.In a separate experiment, single freeze-dried fibres were used to determine the relationship between their ATP content and apparentK _m for ATP. There was a tendency for high ATP concentrations in fibres with highK _m values.When myofibrillar ATPase activity was related to the maximum velocity of shortening of the five fibre types, a significant correlation was found. It is concluded that calcium-stimulated myofibrillar ATPase histochemistry allows an estimate of the maximum shortening velocity of muscle fibres fromXenopus laevis.     

The induction of chromosomal damage in rat hepatocytes and lymphocytes II. Alkylation damage and repair of rat-liver DNA after diethylnitrosamine,dimethylnitrosamine and ethyl methanesulphonate in relation to clastogenic effects

Rat-liver DNA alkylation by diethylnitrosamine (DEN), dimethylnitrosamine (DMN) and ethyl methanesulphonate (EMS) was studied in an attempt to relate chromosome-damaging effects of these agents (the formation of micronuclei in hepatocytes; see preceding paper) to specific alkylation patterns. No correlation was observed between the induction of micronuclei and liver DNA N-alkylation, measured as 3- and 7-alkyl-purines. O⁶-Alkylguanine is probably not involved in micronucleus induction because it is lost from DNA too rapidly to explain the much more persistent clastogenic effects. In contrast, both the initial amounts of alkylphosphotriesters and the persistencies of these products roughly paralleled the respective effects on micronucleus induction. The possible involvement of alkylphosphotriesters or other O-alkylation products of comparable stabilities is discussed. Results with DMN suggest that part of the primary DNA methylation damage is converted into a secondary (DNA) lesion and that both the primary and secondary lesion(s) contribute to the process of micronucleus formation.