From a laboratory stock of Drosophila melanogaster (Oregon), reared for more than 20 years at 18°C, two new populations were derived and maintained at 25° and 28°C for 8 years. The chromosomal and cytoplasmic contribution to genetic divergence between the two more extreme populations was estimated at 18°C and 28°C. Wing shape and two fitness components (fecundity and fertility) were taken into account. Fourier descriptors and the position of the centroid were taken as indicators either of wing shape variation, determined by a different response of the two wing compartments to temperature selection, or of wing shape variation determined by both compartments. The descriptors appear to be good characters: they show a variability which is genetically controlled and ascribable to genes located on specific chromosomes. The third chromosome is responsible for the adaptive difference to temperature. The genes which control wing shape are located on the second and third chromosome, although the contribution of each chromosome depends on the environment in which the flies develop. Cytoplasmic genes display an effect as large as that of chromosomes, and nucleus × cytoplasm interaction is present. The correlation between the genetic contributions to compartment‐dependent wing shape variation and the contributions to fitness is highly significant, especially at 28°C. Wing shape has, therefore, an adaptive significance in relation to temperature, which is particularly expressed in the environment where selection occurred.
From a laboratory stock of Drosophila melanogaster (Oregon), reared for more than 20 years at 18" C, a new population was derived and maintained at 28" C for 8 years. The chromosomal and cytoplasmic contribution to genetic divergence between the two populations was estimated. Six body traits and reproductive fitness were taken into account. The third chromosome is responsible for the adaptive difference for temperature between the two lines. Temperature-selected genes which control body size are located on the second and third chromosomes, although the contribution of each chromosome depends on the environment in which the flies develop. The correlation between the chromosomal and cytoplasmic contributions to different traits and fitness, changes with temperature. At 28" C the correlation between fitness and each body trait is proportional to the response to selection exhibited by each of them, but this is not true at 18" C. Body size has, therefore, an adaptive significance in relation to temperature, which is expressed only in the environment where selection occurs. Cytoplasmic genes affect almost all characters to an extent similar to that of chromosomal genes. Inter-chromosomal and nucleocytoplasmic interactions are present and also change with temperature. In general, genes selected in a given environment produce greater phenotypic changes in that environment than in another. The population that experienced both temperatures is fitter in both environments, suggesting that the capacity to adapt to warm temperatures depends on genes other than those which are involved in the adaptation to cold. 235 236
We have studied several cell behaviour parameters of mutant alleles of fat (ft) in Drosophila imaginal wing disc development. Mutant imaginal discs continue growing in larvae delayed in pupariation and can reach sizes of several times those of wild-type. Their growth is, however, basically allometric. Homozygous ft cells grow faster than their twin cells in clones and generate larger territories, albeit delimited by normal clonal restrictions. Moreover, ft cells in clones tend to grow towards wing proximal regions. These behaviours can be related with failures in cell adhesiveness and cell recognition. Double mutant combinations with alleles of other genes, e.g. of the Epidermal growth factor receptor (DER) pathway, modify ft clonal phenotypes, indicating that adhesiveness is modulated by intercellular signalling. Mutant ft cells show, in addition, smaller cell sizes during proliferation and abnormal cuticular differentiation, which reflect cell membrane and cytoskeleton anomalies, which are not modulated by the DER pathway.
We investigated the heat tolerance of adults of three replicated lines of Drosophila melanogaster that have been evolving independently by laboratory natural selection for 15 yr at "nonextreme" temperatures (18°C, 25°C, or 28°C). These lines are known to have diverged in body size and in the thermal dependence of several life-history traits. Here we show that they differ also in tolerance of extreme high temperature as well as in induced thermotolerance ("heat hardening"). For example, the 28°C flies had the highest probability of surviving a heat shock, whereas the 18°C flies generally had the lowest probability. A short heat pretreatment increased the heat tolerance of the 18°C and 25°C lines, and the threshold temperature necessary to induce thermotolerance was lower for the 18°C line than for the 25°C line. However, neither heat pretreatment nor acclimation to different temperatures influenced heat tolerance of the 28°C line, suggesting the loss of capacity for induced thermotolerance and for acclimation. Thus, patterns of tolerance of extreme heat, of acclimation, and of induced thermotolerance have evolved as correlated responses to natural selection at nonextreme temperatures. A genetic analysis of heat tolerance of a representative replicate population each from the 18°C and 28°C lines indicates that chromosomes 1, 2, and 3 have significant effects on heat tolerance. However, the cytoplasm has little influence, contrary to findings in an earlier study of other stocks that had been evolving for 7 yr at 14°C versus 25°C. Because genes for heat stress proteins (hsps) are concentrated on chromosome 3, the potential role of hsps in the heat tolerance and of induced thermotolerance in these naturally selected lines is currently unclear. In any case, species of Drosophila possess considerable genetic variation in thermal sensitivity and thus have the potential to evolve rapidly in response to climate change; but predicting that response may be difficult.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.