We present data on the relationship between the rate of transposition and copy number in the genome for the copia and Doc retrotransposons of Drosophila melanogaster. copia and Doc transposition rates were directly measured in sublines of the isogenic 2b line using individual males or females, respectively, with a range of copia copy numbers from 49 to 103 and Doc copy numbers from 112 to 235 per genome. Transposition rates varied from 3×10−4 to 2×10−2 for copia and from 2×10−4 to 2×10−3 for Doc. A positive relationship between transposition rate and copy number was found both for copia and for Doc when the data were analysed across all the 2b individuals; no significant correlation was found when the data were analysed across the subline means for both retrotransposons tested. Overall, correlation between copia and Doc transposition rate and their copy number in the genome, if any, was not negative, which would be expected if transposable elements (TEs) self-regulate their copy number. Thus, for copia and Doc no evidence for self-regulation was provided, and at least for these two TEs this hypothesis is not favoured for explaining the maintenance of the stable copy number that is characteristic for natural populations. The transposition rate of copia was measured twice, and a strong positive correlation between copy number and transposition rate both across individuals and subline means was found in 1994, while in 1995 no correlation was found. This fact is in agreement with the hypothesis that a positive correlation between the rate of transposition and TE copy number may be a default starting point for future host–TE coevolution.

To test whether stressful conditions altered levels of heritable variation in fecundity in Drosophila melanogaster, parent–offspring comparisons were undertaken across three generations for flies reared in a combined stress (ethanol, cold shock, low nutrition) environment or a control environment. The stressful conditions did not directly influence fecundity but did lead to a reduced fecundity in the offspring generations, perhaps reflecting cross-generation maternal effects. Both the heritability and evolvability estimates were higher in the combined stress treatment, reflecting an apparent increase in the additive genetic variance under stress. In contrast, there were no consistent changes in the environmental variance across environments.

A set of Drosophila melanogaster was generated, all derived from a common isogenic base stock and each with a single new P element insert on the second or third chromosome. The lines were scored for their body size, measured as thorax length. P inserts were associated with highly significant effects on body size, although the genotypes of the construct and of the control prevented deduction of the direction of mutant effects. In addition to mutant effects on the thorax length of both sexes, there were also highly significant sex-specific effects. Pleiotropic effects of inserts affecting body size on viability and bristle number, as ascertained in a separate study of these lines (Lyman et al., 1996), were weak. Insertional mutagenesis is potentially a powerful tool for investigating the genes involved in size-control in Drosophila, but the technique requires fine tuning for use on polygenic and fitness-related traits.

We investigated three aspects of adaptation to variable environments in Daphnia pulex (Cladocera: Crustacea): (1) effects of temporal variation on the evolution of phenotypic plasticity ; (2) plasticity in sexual versus asexual lineages; (3) maintenance of genetic variation in variable environments. We performed a 72-day quasi-natural selection experiment comparing three patterns of variation: constant temperatures, varying but predictable temperature change, and unpredictable temperature change. All populations were begun with an identical array of 34 clones. During selection clonal variation declined in all populations and different patterns of environmental variation had little effect on amounts of genetic variation. Sexual and asexual lineages differed in size and growth rate, but did not differ in amounts of plasticity or in adaptation to variable environments. The primary target of selection was the Malthusian parameter (r) and life history traits of development time, offspring size and offspring number. The heritability of plasticity was generally lower than trait heritability. Because of this difference, the selection response on the mean of the traits overwhelmed the selection response on plasticity. Lower heritabilities of plasticity are very typical, suggesting that our results will be typical of responses to selection in nature. Our results suggest that selection will act mostly on trait means within environments and that plasticity will evolve often as a correlated trait. Because selection on plasticity is based on its across-deme, global fitness, this process will usually be slow. Comparative studies need to shift from closely related, local population differences to those of more distantly related populations or even different species.

A study was undertaken to test whether the elimination of metabolic pathways strongly involved in growth and fatness, comprising thyroid hormones (TH) and growth hormone (GH), is responsible for a substantial part of the genetic change produced by selection. Lines used in this study have been selected for about 50 generations for high (PH) and low (PL) body weight at 10 weeks and for high (F) and low fat content (L) at 14 weeks, producing a 3-fold difference in body weights and a 5-fold difference in fat content. Thyroid ablation was achieved by repeated backcrossing into the four selection lines of a transgene comprising the HSV1-tk gene coupled to the promoter of the thyroglobulin gene. Hemizygous pregnant dams were treated with ganciclovir leading to thyroid-ablated dams and offspring and therefore to a lack of TH and subsequently of GH. In the absence of TH and GH, lines still differ in body weight over the period studied (10 d to about 100 d; e.g. at the end PH=32·1 g vs PL=10·2 g) and in fat content (F=16·2% vs L=3·8%) ; the corresponding values for the wild-type controls were PH=49·9 g vs PL=17·4 g and F=27·5% vs L=4·8%. The effect of the transgene depended on the genetic background for body weights at most ages and for relative gonadal fat pad weights, but less for fat content. The L line showed the lowest growth depression. The lit gene, which causes GH but not TH deficiency, was also transferred by repeated backcrosses into three of these lines (PH, PL, F). The combined deficiency of TH and GH had bigger effects on body weights at earlier ages than did GH deprivation. The data show that changes in the TH- and GH-systems are not the only cause of line differences in growth and fatness resulting from long-term selection, but both are involved to a significant extent. The interactions between the effects of the transgene and of the lit gene and the genetic background were, nevertheless, relatively small and therefore these results support a polygenic model of selection response.

Formulae are given for computing the distribution of numbers of selected individuals of each genotype and thus change in gene frequency at a locus with a large effect on a quantitative trait under truncation selection in a finite population. Results are illustrated with respect to use of selection for quantitative trait locus (QTL) detection, specifically by bulk segregant analysis with linked markers, for which probabilities that selected samples will comprise almost all one genotypic class are computed.