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• Parallel evolution of similar morphologies in closely related lineages provides insight into the repeatability and predictability of evolution. In the genus Antirrhinum (snapdragons), as in other plants, a suite of morphological characters are associated with adaptation to alpine environments. • We tested for parallel trait evolution in Antirrhinum by investigating phylogenetic relationships using restriction-site associated DNA (RAD) sequencing. We then associated phenotypic information to our phylogeny to reconstruct the patterns of morphological evolution and related this to evidence for hybridisation between emergent lineages. • Phylogenetic analyses showed that the alpine character syndrome is present in multiple groups, suggesting that Antirrhinum has repeatedly colonised alpine habitats. Dispersal to novel environments happened in the presence of intraspecific and interspecific gene flow. • We found support for a model of parallel evolution in Antirrhinum. Hybridisation in natural populations, and a complex genetic architecture underlying the alpine morphology syndrome, support an important role of natural selection in maintaining species divergence in the face of gene flow.

Similar morphological, physiological, and behavioral features have evolved independently in different species, a pattern known as convergence. It is known that morphological convergence can occur through changes in orthologous genes. In some cases of convergence, cis -regulatory changes generate parallel modifications in the expression patterns of orthologous genes. Our understanding of how changes in cis -regulatory regions contribute to convergence is hampered, usually, by a limited understanding of the global cis -regulatory structure of the evolving genes. Here we examine the genetic causes of a case of precise phenotypic convergence between Drosophila sechellia and Drosophila ezoana , species that diverged ∼ 40 Mya. Previous studies revealed that changes in multiple transcriptional enhancers of shavenbaby (svb , a transcript of the ovo locus) caused phenotypic evolution in the D. sechellia lineage. It has also been shown that the convergent phenotype of D. ezoana was likely caused by cis -regulatory evolution of svb . Here we show that the large-scale cis- regulatory architecture of svb is conserved between these Drosophila species. Furthermore, we show that the D. ezoana orthologs of the evolved D. sechellia enhancers have also evolved expression patterns that correlate precisely with the changes in the phenotype. Our results suggest that phenotypic convergence resulted from multiple noncoding changes that occurred in parallel in the D. sechellia and D. ezoana lineages.

Parallel evolution across replicate populations has provided evolutionary biologists with iconic examples of adaptation. When multiple populations colonize seemingly similar habitats, they may evolve similar genes, traits, or functions. Yet, replicated evolution in nature or in the laboratory often yields inconsistent outcomes: Some replicate populations evolve along highly similar trajectories, whereas other replicate populations evolve to different extents or in distinct directions. To understand these heterogeneous outcomes, biologists are increasingly treating parallel evolution not as a binary phenomenon but rather as a quantitative continuum ranging from parallel to nonparallel. By measuring replicate populations' positions along this (non)parallel continuum, we can test hypotheses about evolutionary and ecological factors that influence the extent of repeatable evolution. We review evidence regarding the manifestation of (non)parallel evolution in the laboratory, in natural populations, and in applied contexts such as cancer. We enumerate the many genetic, ecological, and evolutionary processes that contribute to variation in the extent of parallel evolution.

The evolution of herbicide resistance in crop weeds presents one of the greatest challenges to agriculture and the production of food. Herbicide resistance has been studied for more than 60 yr, in the large part by researchers seeking to design effective weed control programs. As an outcome of this work, various unique questions in plant adaptation have been addressed. Here, I collate recent research on the herbicide-resistant problem in light of key questions and themes in evolution and ecology. I highlight discoveries made on herbicide-resistant weeds in three broad areas – the genetic basis of adaptation, evolutionary constraints, experimental evolution – and similarly discuss questions left to be answered. I then develop how one would use herbicideresistance evolution as a model for studying eco-evolutionary dynamics within a community context. My overall goals are to highlight important findings in the weed science literature that are relevant to themes in plant adaptation and to stimulate the use of herbicide-resistant plants as models for addressing key questions within ecology and evolution.

Population genetic theory predicts that effective population size and gene flow can strongly influence the levels and patterns of genetic variability, and thereby also the likelihood, pace and direction of evolutionary transformations. Given that levels and patterns of genetic variability in lakes and ponds often differ from those observed in continuous marine environments, it follows that the dynamics of adaptation and evolution in freshwater habitats are also likely to differ from those in marine habitats. Here, I explore and discuss some ideas relating to the likelihood of parallel phenotypic evolution through similar (parallel) vs. different (convergent) genetic changes with particular focus on freshwater isolates. I will review and discuss the available genetic data with particular focus on freshwater fish populations, and outline possible avenues for future work in which ponds and small lakes could serve as useful model systems to study genetic parallelism and convergence, as well as molecular adaptation in general. Conservation issues related to genetics of isolated pond and lake populations are also addressed.

Genomic and genetic methods allow investigation of how frequently the same genes are used by different populations during adaptive evolution, yielding insights into the predictability of evolution at the genetic level. We estimated the probability of gene reuse in parallel and convergent phenotypic evolution in nature using data from published studies. The estimates are surprisingly high, with mean probabilities of 0.32 for genetic mapping studies and 0.55 for candidate gene studies. The probability declines with increasing age of the common ancestor of compared taxa, from about 0.8 for young nodes to 0.1–0.4 for the oldest nodes in our study. Probability of gene reuse is higher when populations begin from the same ancestor (genetic parallelism) than when they begin from divergent ancestors (genetic convergence). Our estimates are broadly consistent with genomic estimates of gene reuse during repeated adaptation to similar environments, but most genomic studies lack data on phenotypic traits affected. Frequent reuse of the same genes during repeated phenotypic evolution suggests that strong biases and constraints affect adaptive evolution, resulting in changes at a relatively small subset of available genes. Declines in the probability of gene reuse with increasing age suggest that these biases diverge with time.

Evidence of phenotypic parallelism is often used to infer the deterministic role played by natural selection. However, variation in the extent or direction of divergence is often evident among independent evolutionary replicates, raising the following question: just how parallel, overall, is parallel evolution? We answer this question through a comparative analysis of studies of fishes, a taxon where parallel evolution has been much discussed. We first ask how much of the among-population variance in phenotypic traits can be explained by different “environment” types, such as high predation versus low predation or benthic versus limnetic. We then use phenotypic change vector analysis to quantify variation in the direction (vector angles) and magnitude (vector lengths) of environment-associated divergence. All analyses show high variation in the extent of parallelism—from very high to very low, along with everything in between—highlighting the importance of quantifying parallelism rather than just asserting its presence. Interestingly, instances of low extents of parallelism represent important components of divergence in many cases, promising considerable opportunities for inferences about the factors shaping phenotypic divergence.

Aneuploidy, chromosomal instability, somatic copy-number alterations, and whole-genome doubling (WGD) play key roles in cancer evolution and provide information for the complex task of phylogenetic inference. We present MEDICC2, a method for inferring evolutionary trees and WGD using haplotype-specific somatic copy-number alterations from single-cell or bulk data. MEDICC2 eschews simplifications such as the infinite sites assumption, allowing multiple mutations and parallel evolution, and does not treat adjacent loci as independent, allowing overlapping copy-number events. Using simulations and multiple data types from 2780 tumors, we use MEDICC2 to demonstrate accurate inference of phylogenies, clonal and subclonal WGD, and ancestral copy-number states.

Selfing has evolved in animals, fungi, and plants, and since Darwin's pioneering study, it is considered one of the most frequent evolutionary trends in flowering plants. Generally, the evolution of selfing is characterized by a loss of self-incompatibility, the selfing syndrome, and changes in genome-wide polymorphism patterns. Recent interdisciplinary studies involving molecular functional experiments, genome-wide data, experimental evolution, and evolutionary ecology using Arabidopsis thaliana, Caenorhabditis elegans , and other species show that the evolution of selfing is not merely a degradation of outcrossing traits but a model for studying the recurrent patterns underlying adaptive molecular evolution. For example, in wild Arabidopsis relatives, self-compatibility evolved from mutations in the male specificity gene, S-LOCUS CYSTEINE-RICH PROTEIN S-LOCUS PROTEIN 11 ( SCR SP11 ), rather than the female specificity gene, S-LOCUS RECEPTOR KINASE ( SRK ), supporting the theoretical prediction of sexual asymmetry. Prevalence of dominant self-compatible mutations is consistent with Haldane's sieve, which acts against recessive adaptive mutations. Time estimates based on genome-wide polymorphisms and self-incompatibility genes generally support the recent origin of selfing.

Antibiotic resistance is a growing health concern. Efforts to control resistance would benefit from an improved ability to forecast when and how it will evolve. Epistatic interactions between mutations can promote divergent evolutionary trajectories, which complicates our ability to predict evolution. We recently showed that differences between genetic backgrounds can lead to idiosyncratic responses in the evolvability of phenotypic resistance, even among closely related Escherichia coli strains. In this study, we examined whether a strain’s genetic background also influences the genotypic evolution of resistance. Do lineages founded by different genotypes take parallel or divergent mutational paths to achieve their evolved resistance states? We addressed this question by sequencing the complete genomes of antibiotic-resistant clones that evolved from several different genetic starting points during our earlier experiments. We first validated our statistical approach by quantifying the specificity of genomic evolution with respect to antibiotic treatment. As expected, mutations in particular genes were strongly associated with each drug. Then, we determined that replicate lines evolved from the same founding genotypes had more parallel mutations at the gene level than lines evolved from different founding genotypes, although these effects were more subtle than those showing antibiotic specificity. Taken together with our previous work, we conclude that historical contingency can alter both genotypic and phenotypic pathways to antibiotic resistance.