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Morphological traits often covary within and among species according to simple power laws referred to as allometry. Such allometric relationships may result from common growth regulation, and this has given rise to the hypothesis that allometric exponents may have low evolvability and constrain trait evolution. We formalize hypotheses for how allometry may constrain morphological trait evolution across taxa, and test these using more than 300 empirical estimates of static (within-species) allometric relations of animal morphological traits. Although we find evidence for evolutionary changes in allometric parameters on million-year, cross-species time scales, there is limited evidence for microevolutionary changes in allometric slopes. Accordingly, we find that static allometries often predict evolutionary allometries on the subspecies level, but less so across species. Although there is a large body of work on allometry in a broad sense that includes all kinds of morphological trait–size relationships, we found relatively little information about the evolution of allometry in the narrow sense of a power relationship. Despite the many claims of microevolutionary changes of static allometries in the literature, hardly any of these apply to narrow-sense allometry, and we argue that the hypothesis of strongly constrained static allometric slopes remains viable.

Defensins are a well-characterised group of small, disulphide-rich, cationic peptides that are produced by essentially all eukaryotes and are highly diverse in their sequences and structures. Most display broad range antimicrobial activity at low micromolar concentrations, whereas others have other diverse roles, including cell signalling (e.g. immune cell recruitment, self/non-self-recognition), ion channel perturbation, toxic functions, and enzyme inhibition. The defensins consist of two superfamilies, each derived from an independent evolutionary origin, which have subsequently undergone extensive divergent evolution in their sequence, structure and function. Referred to as the cis - and trans -defensin superfamilies, they are classified based on their secondary structure orientation, cysteine motifs and disulphide bond connectivities, tertiary structure similarities and precursor gene sequence. The utility of displaying loops on a stable, compact, disulphide-rich core has been exploited by evolution on multiple occasions. The defensin superfamilies represent a case where the ensuing convergent evolution of sequence, structure and function has been particularly extreme. Here, we discuss the extent, causes and significance of these convergent features, drawing examples from across the eukaryotes.

Behaviours are often correlated within broader syndromes, creating the potential for evolution in one behaviour to drive evolutionary changes in other behaviours. Despite demonstrations that behavioural syndromes are common, this potential for evolutionary effects has not been demonstrated. Here we show that populations of field crickets ( Gryllus integer ) exhibit a genetically conserved behavioural syndrome structure, despite differences in average behaviours. We found that the distribution of genetic variation and genetic covariance among behavioural traits was consistent with genes and cellular mechanisms underpinning behavioural syndromes rather than correlated selection. Moreover, divergence among populations' average behaviours was constrained by the genetically conserved behavioural syndrome. Our results demonstrate that a conserved genetic architecture linking behaviours has shaped the evolutionary trajectories of populations in disparate environments—illustrating an important way for behavioural syndromes to result in shared evolutionary fates.

The defensin and defensin-like proteins are an extensive group of small, cationic, disulfide-rich proteins found in animals, plants, and fungi and mostly perform roles in host defense. The term defensin was originally used for small mammalian proteins found in neutrophils and was subsequently applied to insect proteins and plant γ-thionins based on their perceived sequence and structural similarity. Defensins are often described as ancient innate immunity molecules and classified as a single superfamily and both sequence alignments and phylogenies have been constructed. Here, we present evidence that the defensins have not all evolved from a single ancestor. Instead, they consist of two analogous superfamilies, and extensive convergent evolution is the source of their similarities. Evidence of common origin necessarily gets weaker for distantly related genes, as is the case for defensins, which are both divergent and small. We show that similarities that have been used as evidence for common origin are all expected by chance in short, constrained, disulfide-rich proteins. Differences in tertiary structure, secondary structure order, and disulfide bond connectivity indicate convergence as the likely source of the similarity. We refer to the two evolutionarily independent groups as the cis-defensins and trans-defensins based on the orientation of the most conserved pair of disulfides.

One of the most important shifts in evolutionary biology in the past 50 years is an increased recognition of sluggish evolution and failures to adapt, which seem paradoxical in view of abundant genetic variation and many instances of rapid local adaptation. I review hypotheses of evolutionary constraint (or restraint), and suggest that although constraints on individual characters or character complexes may often reside in the structure or paucity of genetic variation, organism-wide stasis, as described by paleontologists, might better be explained by a hypothesis of ephemeral divergence, according to which the spatial or temporal divergence of populations is often short-lived because of interbreeding with nondivergent populations. Among the many consequences of acknowledging evolutionary constraints, community ecology is being transformed as it takes into account phylogenetic niche conservatism and the strong imprint of deep history.

Abstract Variability in expression levels in response to random genomic mutations varies among genes, influencing both the facilitation and constraint of phenotypic evolution in organisms. Despite its importance, both the underlying mechanisms and evolutionary origins of this variability remain largely unknown due to the mixed contributions of cis- and trans-acting elements. To address this issue, we focused on the mutational variability of cis-acting elements, that is, promoter regions, in Escherichia coli. Random mutations were introduced into the natural and synthetic promoters to generate mutant promoter libraries. By comparing the variance in promoter activity of these mutant libraries, we found no significant difference in mutational variability in promoter activity between promoter groups, suggesting the absence of a signature of natural selection for mutational robustness. In contrast, the promoters controlling essential genes exhibited a remarkable bias in mutational variability, with mutants displaying higher activities than the wild types being relatively rare compared to those with lower activities. Our evolutionary simulation on a rugged fitness landscape provided a rationale for this vulnerability. These findings suggest that past selection created nonuniform mutational variability in promoters biased toward lower activities of random mutants, which now constrains the future evolution of downstream essential genes toward higher expression levels.

Phenotypically plastic genotypes express different phenotypes in different environments, often in adaptive ways. The evolution of phenotypic plasticity creates developmental systems that are more flexible along the trait dimensions that are more plastic, and as a result, we hypothesize that such traits will express greater mutational variance, genetic variance, and evolvability. We develop an explicit gene network model with three components: some genes can receive environmental cues about the adult selective environment, some genes that interact repeatedly to determine each others' final state, and other factors that translate these final expression states into the phenotype. We show that the evolution of phenotypic plasticity is an important determinant of mutational patterns, genetic variance, and evolutionary potential of a population. Phenotypic plasticity tends to lead to populations with greater mutational variance, greater standing genetic variance, and, when the optimal phenotypes of two traits vary in concert, greater mutational and genetic correlations. However, plastic populations do not tend to respond much more rapidly to selection than do populations evolved in a static environment. We find that the quantitative genetic descriptions of traits created by explicit developmental network models are evolutionarily labile, with genetic correlations that change rapidly with shifts in the selection regime.

• The evolution of herbicide resistance in weeds is an example of parallel evolution, through which genes encoding herbicide target proteins are repeatedly represented as evolutionary targets. The number of herbicide target-site genes differs among species, and little is known regarding the effects of duplicate gene copies on the evolution of herbicide resistance. • We investigated the evolution of herbicide resistance in Monochoria vaginalis, which carries five copies of sulfonylurea target-site acetolactate synthase (ALS) genes. Suspected resistant populations collected across Japan were investigated for herbicide sensitivity and ALS gene sequences, followed by functional characterization and ALS gene expression analysis. • We identified over 60 resistant populations, all of which carried resistance-conferring amino acid substitutions exclusively in MvALS1 or MvALS3. All MvALS4 alleles carried a loss-of-function mutation. Although the enzymatic properties of ALS encoded by these genes were not markedly different, the expression of MvALS1 and MvALS3 was prominently higher among all ALS genes. • The higher expression of MvALS1 and MvALS3 is the driving force of the biased representation of genes during the evolution of herbicide resistance in M. vaginalis. Our findings highlight that gene expression is a key factor in creating evolutionary hotspots.

An attractive and long-standing hypothesis regarding the evolution of genes after duplication posits that the duplication event creates new evolutionary possibilities by releasing a copy of the gene from constraint. Apparent support was found in numerous analyses, particularly, the observation of higher rates of evolution in duplicated as compared with singleton genes. Could it, instead, be that more duplicable genes (owing to mutation, fixation, or retention biases) are intrinsically faster evolving? To uncouple the measurement of rates of evolution from the determination of duplicate or singleton status, we measure the rates of evolution in singleton genes in outgroup primate lineages but classify these genes as to whether they have duplicated or not in a crown group of great apes. We find that rates of evolution are higher in duplicable genes prior to the duplication event. In part this is owing to a negative correlation between coding sequence length and rate of evolution, coupled with a bias toward smaller genes being more duplicable. The effect is masked by difference in expression rate between duplicable genes and singletons. Additionally, in contradiction to the classical assumption, we find no convincing evidence for an increase in dN/dS after duplication, nor for rate asymmetry between duplicates. We conclude that high rates of evolution of duplicated genes are not solely a consequence of the duplication event, but are rather a predictor of duplicability. These results are consistent with a model in which successful gene duplication events in mammals are skewed toward events of minimal phenotypic impact.

We review the evolutionary importance of developmental mechanisms in constraining evolutionary changes in animals-in other words, developmental constraints. We focus on hard constraints that can act on macroevolutionary timescales. In particular, we discuss the causes and evolutionary consequences of the ancient metazoan constraint that differentiated cells cannot divide and constraints against changes of phylotypic stages in vertebrates and other higher taxa. We conclude that in all cases these constraints are caused by complex and highly controlled global interactivity of development, the disturbance of which has grave consequences. Mutations that affect such global interactivity almost unavoidably have many deleterious pleiotropic effects, which will be strongly selected against and will lead to long-term evolutionary stasis. The discussed developmental constraints have pervasive consequences for evolution and critically restrict regeneration capacity and body plan evolution.