Divergent selection and phenotypic plasticity during incipient speciation in Lake Victoria cichlid fish

Divergent selection acting on several different traits that cause multidimensional shifts are supposed to promote speciation, but the outcome of this process is highly dependent on the balance between the strength of selection vs. gene flow. Here, we studied a pair of sister species of Lake Victoria cichlids at a location where they hybridize and tested the hypothesis that divergent selection acting on several traits can maintain phenotypic differentiation despite gene flow. To explore the possible role of selection we tested for correlations between phenotypes and environment and compared phenotypic divergence (P-ST) with that based on neutral markers (F-ST). We found indications for disruptive selection acting on male breeding colour and divergent selection acting on several morphological traits. By performing common garden experiments we also separated the environmental and heritable components of divergence and found evidence for phenotypic plasticity in some morphological traits contributing to species differences.

Epigenetic variation creates potential for evolution of plant phenotypic plasticity

Heritable variation in plant phenotypes, and thus potential for evolutionary change, can in principle not only be caused by variation in DNA sequence, but also by underlying epigenetic variation. However, the potential scope of such phenotypic effects and their evolutionary significance are largely unexplored. Here, we conducted a glasshouse experiment in which we tested the response of a large number of epigenetic recombinant inbred lines (epiRILs) of Arabidopsis thaliana – lines that are nearly isogenic but highly variable at the level of DNA methylation – to drought and increased nutrient conditions. We found significant heritable variation among epiRILs both in the means of several ecologically important plant traits and in their plasticities to drought and nutrients. Significant selection gradients, that is, fitness correlations, of several mean traits and plasticities suggest that selection could act on this epigenetically based phenotypic variation. Our study provides evidence that variation in DNA methylation can cause substantial heritable variation of ecologically important plant traits, including root allocation, drought tolerance and nutrient plasticity, and that rapid evolution based on epigenetic variation alone should thus be possible.

Ecological speciation and phenotypic plasticity affect ecosystems

Phenotypic differences among closely related populations and species can cause contrasting effects on ecosystems; however, it is unknown whether such effects result from genetic divergence, phenotypic plasticity, or both. To test this, we reared sympatric limnetic and benthic species of whitefish from a young adaptive radiation in a common garden, where the benthic species was raised on two distinct food types. We then used these fish in a mesocosm experiment to test for contrasting ecosystem effects of closely related species and of plastically induced differences within a species. We found that strong contrasting ecosystem effects resulted more frequently from genetic divergence, although they were not stronger overall than those resulting from phenotypic plasticity. Overall, our results provide evidence that genetically based differences among closely related species that evolved during a young adaptive radiation can affect ecosystems, and that phenotypic plasticity can modify the ecosystem effects of such species.

Disentangling the role of phenotypic plasticity and genetic divergence in contemporary ecotype formation during a biological invasion

The occurrence of contemporary ecotype formation through adaptive divergence of populations within the range of an invasive species typically requires standing genetic variation but can be facilitated by phenotypic plasticity. The relative contributions of both of these to adaptive trait differentiation have rarely been simultaneously quantified in recently diverging vertebrate populations. Here we study a case of intraspecific divergence into distinct lake and stream ecotypes of threespine stickleback that evolved in the past 140 years within the invasive range in Switzerland. Using a controlled laboratory experiment with full-sib crosses and treatments mimicking a key feature of ecotypic niche divergence, we test if the phenotypic divergence that we observe in the wild results from phenotypic plasticity or divergent genetic predisposition. Our experimental groups show qualitatively similar phenotypic divergence as those observed among wild adults. The relative contribution of plasticity and divergent genetic predisposition differs among the traits studied, with traits related to the biomechanics of feeding showing a stronger genetic predisposition, whereas traits related to locomotion are mainly plastic. These results implicate that phenotypic plasticity and standing genetic variation interacted during contemporary ecotype formation in this case.

Phenotypic plasticity is a negative, though weak, predictor of the commonness of 105 grassland species

Aim The usual hypothesis about the relationship between niche breadth and range size posits that species with the capacity to use a wider range of resources or to tolerate a greater range of environmental conditions should be more widespread. In plants, broader niches are often hypothesized to be due to pronounced phenotypic plasticity, and more plastic species are therefore predicted to be more common. We examined the relationship between the magnitude of phenotypic plasticity in five functional traits, mainly related to leaves, and several measures of abundance in 105 Central European grassland species. We further tested whether mean values of traits, rather than their plasticity, better explain the commonness of species, possibly because they are pre-adapted to exploiting the most common resources. Location Central Europe. Methods In a multispecies experiment with 105 species we measured leaf thickness, leaf greenness, specific leaf area, leaf dry matter content and plant height, and the plasticity of these traits in response to fertilization, waterlogging and shading. For the same species we also obtained five measures of commonness, ranging from plot-level abundance to range size in Europe. We then examined whether these measures of commonness were associated with the magnitude of phenotypic plasticity, expressed as composite plasticity of all traits across the experimental treatments. We further estimated the relative importance of trait plasticity and trait means for abundance and geographical range size. Results More abundant species were less plastic. This negative relationship was fairly consistent across several spatial scales of commonness, but it was weak. Indeed, compared with trait means, plasticity was relatively unimportant for explaining differences in species commonness. Main conclusions Our results do not indicate that larger phenotypic plasticity of leaf morphological traits enhances species abundance. Furthermore, possession of a particular trait value, rather than of trait plasticity, is a more important determinant of species commonness.

Molecular mechanisms of muscle plasticity with exercise

The skeletal muscle phenotype is subject to considerable malleability depending on use. Low-intensity endurance type exercise leads to qualitative changes of muscle tissue characterized mainly by an increase in structures supporting oxygen delivery and consumption. High-load strength-type exercise leads to growth of muscle fibers dominated by an increase in contractile proteins. In low-intensity exercise, stress-induced signaling leads to transcriptional upregulation of a multitude of genes with Ca2+ signaling and the energy status of the muscle cells sensed through AMPK being major input determinants. Several parallel signaling pathways converge on the transcriptional co-activator PGC-1α, perceived as being the coordinator of much of the transcriptional and posttranscriptional processes. High-load training is dominated by a translational upregulation controlled by mTOR mainly influenced by an insulin/growth factor-dependent signaling cascade as well as mechanical and nutritional cues. Exercise-induced muscle growth is further supported by DNA recruitment through activation and incorporation of satellite cells. Crucial nodes of strength and endurance exercise signaling networks are shared making these training modes interdependent. Robustness of exercise-related signaling is the consequence of signaling being multiple parallel with feed-back and feed-forward control over single and multiple signaling levels. We currently have a good descriptive understanding of the molecular mechanisms controlling muscle phenotypic plasticity. We lack understanding of the precise interactions among partners of signaling networks and accordingly models to predict signaling outcome of entire networks. A major current challenge is to verify and apply available knowledge gained in model systems to predict human phenotypic plasticity.

Caenorhabditis elegans Heterochromatin protein 1 (HPL-2) links developmental plasticity, longevity and lipid metabolism

Background Heterochromatin protein 1 (HP1) family proteins have a well-characterized role in heterochromatin packaging and gene regulation. Their function in organismal development, however, is less well understood. Here we used genome-wide expression profiling to assess novel functions of the Caenorhabditis elegans HP1 homolog HPL-2 at specific developmental stages. Results We show that HPL-2 regulates the expression of germline genes, extracellular matrix components and genes involved in lipid metabolism. Comparison of our expression data with HPL-2 ChIP-on-chip profiles reveals that a significant number of genes up- and down-regulated in the absence of HPL-2 are bound by HPL-2. Germline genes are specifically up-regulated in hpl-2 mutants, consistent with the function of HPL-2 as a repressor of ectopic germ cell fate. In addition, microarray results and phenotypic analysis suggest that HPL-2 regulates the dauer developmental decision, a striking example of phenotypic plasticity in which environmental conditions determine developmental fate. HPL-2 acts in dauer at least partly through modulation of daf-2/IIS and TGF-β signaling pathways, major determinants of the dauer program. hpl-2 mutants also show increased longevity and altered lipid metabolism, hallmarks of the long-lived, stress resistant dauers. Conclusions Our results suggest that the worm HP1 homologue HPL-2 may coordinately regulate dauer diapause, longevity and lipid metabolism, three processes dependent on developmental input and environmental conditions. Our findings are of general interest as a paradigm of how chromatin factors can both stabilize development by buffering environmental variation, and guide the organism through remodeling events that require plasticity of cell fate regulation.

Phenotypic conversion leads to structural and functional changes of smooth muscle sarcolemma

Continuous changes in the length of smooth muscles require a highly organized sarcolemmal structure. Yet, smooth muscle cells also adapt rapidly to altered environmental cues. Their sarcolemmal plasticity must lead to profound changes which affect transmembrane signal transduction as well as contractility. We have established porcine vascular and human visceral smooth muscle cultures of epithelioid and spindle-shaped morphology and determined their plasma membrane properties. Epithelioid cells from both sources contain a higher ratio of cholesterol to glycerophospholipids, and express a less diverse range of lipid-associated annexins. These findings point to a reduction in efficiency of membrane segregation in epithelioid cells. Moreover, compared to spindle-shaped cells, cholesterol is more readily extracted from epithelioid cells with methyl-beta-cyclodextrin and its synthesis is more susceptible to inhibition with lovastatin. The inability of epithelioid cells to process vasoactive metabolites, such as angiotensin or nucleotides further indicates that contractile properties are impaired. Phenotypic plasticity extends beyond the loss of smooth muscle cell marker genes. The plasma membrane has undergone profound functional changes which are incompatible with cyclic foreshortening, but might be important in the development of vascular disease.

Adaptive plasticity and genetic divergence in feeding efficiency during parallel adaptive radiation of whitefish (Coregonus spp.)

Parallel phenotypic divergence in replicated adaptive radiations could either result from parallel genetic divergence in response to similar divergent selec- tion regimes or from equivalent phenotypically plastic response to the repeated occurrence of contrasting environments. In post-glacial fish, repli- cated divergence in phenotypes along the benthic-limnetic habitat axis is commonly observed. Here, we use two benthic-limnetic species pairs of whitefish from two Swiss lakes, raised in a common garden design, with reciprocal food treatments in one species pair, to experimentally measure whether feeding efficiency on benthic prey has a genetic basis or whether it underlies phenotypic plasticity (or both). To do so, we offered experimental fish mosquito larvae, partially burried in sand, and measured multiple feed- ing efficiency variables. Our results reveal both, genetic divergence as well as phenotypically plastic divergence in feeding efficiency, with the pheno- typically benthic species raised on benthic food being the most efficient forager on benthic prey. This indicates that both, divergent natural selection on genetically heritable traits and adaptive phenotypic plasticity, are likely important mechanisms driving phenotypic divergence in adaptive radiation.