Heterochrony and allometry: the analysis of evolutionary change in ontogeny

The connection between development and evolution has become the focus of an increasing amount of research in recent years, and heterochrony has long been a key concept in this relation. Heterochrony is defined as evolutionary change in rates and timing of developmental processes; the dimension of time is therefore an essential part in studies of heterochrony. Over the past two decades, evolutionary biologists have used several methodological frameworks to analyse heterochrony, which differ substantially in the way they characterize evolutionary changes in ontogenies and in the resulting classification, although they mostly use the same terms. This review examines how these methods compare ancestral and descendant ontogenies, emphasizing their differences and the potential for contradictory results from analyses using different frameworks. One of the two principal methods uses a clock as a graphical display for comparisons of size, shape and age at a particular ontogenic stage, whereas the other characterizes a developmental process by its time of onset, rate, and time of cessation. The literature on human heterochrony provides particularly clear examples of how these differences produce apparent contradictions when applied to the same problem. Developmental biologists recently have extended the concept of heterochrony to the earliest stages of development and have applied it at the cellular and molecular scale. This extension brought considerations of developmental mechanisms and genetics into the study of heterochrony, which previously was based primarily on phenomenological characterizations of morphological change in ontogeny. Allometry is the pattern of covariation among several morphological traits or between measures of size and shape; unlike heterochrony, allometry does not deal with time explicitly. Two main approaches to the study of allometry are distinguished, which differ in the way they characterize organismal form. One approach defines shape as proportions among measurements, based on considerations of geometric similarity, whereas the other focuses on the covariation among measurements in ontogeny and evolution. Both are related conceptually and through the use of similar algebra. In addition, there are close connections between heterochrony and changes in allometric growth trajectories, although there is no one-to-one correspondence. These relationships and outline links between different analytical frameworks are discussed.     

Ribosomal DNA and phylogeny of the Ascaridoidea (Nemata: Secernentea): implications for morphological evolution and classification

Nematodes of the superfamily Ascaridoidea are parasites of the alimentary tract of vertebrates and include species that are of medical and economic importance. Existing evolutionary hypotheses for these organisms have frequently been based on interpretation of one or few "key" structural or life history features. We used nuclear-encoded small (1764 characters) and large subunit (757 characters) ribosomal DNA sequences to estimate the phylogeny of representative taxa from this superfamily. Trees inferred by maximum parsimony and maximum likelihood methods strongly support clades that are primarily consistent with one recent classification of the group. In contrast, most previously proposed phylogenetic hypotheses were significantly worse when compared to the maximum likelihood tree by a statistical method. Hypotheses for the evolution of morphological and life history characters were explored by parsimony mapping these features on several tree topologies, including optimal molecular trees and alternative topologies reflecting traditional expectations deemed not worse in statistical tests. The results identify some consistent putative shared-derived morphological features, but also strongly suggest that some key features emphasized by previous workers represent ancestral states or highly homoplastic characters.     

The origins of human ageing

The origins of human ageing are to be found in the origins and evolution of senescence as a general feature in the life histories of higher animals. Ageing is an intriguing problem in evolutionary biology because a trait that limits the duration of life, including the fertile period, has a negative impact on Darwinian fitness. Current theory suggests that senescence occurs because the force of natural selection declines with age and because longevity is only acquired at some metabolic cost. In effect, organisms may trade late survival for enhanced reproductive investments in earlier life. The comparative study of ageing supports the general evolutionary theory and reveals that human senescence, while broadly similar to senescence in other mammalian species, has distinct features, such as menopause, that may derive from the interplay of biological and social evolution.     

Inferring the fitness effects of DNA mutations from polymorphism and divergence data: statistical power to detect directional selection under stationarity and free recombination

The fitness effects of classes of DNA mutations can be inferred from patterns of nucleotide variation. A number of studies have attributed differences in levels of polymorphism and divergence between silent and replacement mutations to the action of natural selection. Here, I investigate the statistical power to detect directional selection through contrasts of DNA variation among functional categories of mutations. A variety of statistical approaches are applied to DNA data simulated under Sawyer and Hartl's Poisson random field model. Under assumptions of free recombination and stationarity, comparisons that include both the frequency distributions of mutations segregating within populations and the numbers of mutations fixed between populations have substantial power to detect even very weak selection. Frequency distribution and divergence tests are applied to silent and replacement mutations among five alleles of each of eight Drosophila simulans genes. Putatively "preferred" silent mutations segregate at higher frequencies and are more often fixed between species than "unpreferred" silent changes, suggesting fitness differences among synonymous codons. Amino acid changes tend to be either rare polymorphisms or fixed differences, consistent with a combination of deleterious and adaptive protein evolution. In these data, a substantial fraction of both silent and replacement DNA mutations appear to affect fitness.     

Population structure in Daphnia obtusa: quantitative genetic and allozymic variation

Quantitative genetic analyses for body size and for life history characters within and among populations of Daphnia obtusa reveal substantial genetic variance at both hierarchical levels for all traits measured. Simultaneous allozymic analysis on the same population samples indicate a moderate degree of differentiation: GST = 0.28. No associations between electrophoretic genotype and phenotypic characters were found, providing support for the null hypothesis that the allozymic variants are effectively neutral. Therefore, GST can be used as the null hypothesis that neutral phenotypic evolution within populations led to the observed differentiation for the quantitative traits, which I call QST. The results of this study provide evidence that natural selection has promoted diversification for body size among populations, and has impeded diversification for relative fitness. Analyses of population differentiation for clutch size, age at reproduction, and growth rate indicate that neutral phenotypic evolution cannot be excluded as the cause.     

Effects of differential selection in the sexes on cytonuclear dynamics. Life stages with sex differences

We extend our investigation of cytonuclear selection by determining when differential selection between the sexes will generate allele frequency changes or cytonuclear disequilibria in populations with constant viability selection and an adult census. We demonstrate analytically that there can be a cytonuclear hitchhiking effect upon a selectively neutral marker in either sex provided the other marker is selected in that sex and there is allelic disequilibrium between the loci in females. Cytonuclear disequilibria are generated de novo in both sexes when both loci affect fitness in females and there is a nonmultiplicative fitness interaction between them. Similar fitness interactions in males generate male disequilibria only. Through numerical analyses, we investigate the potential magnitude of such disequilibria, their qualitative dynamics, the expected frequency of detectable disequilibria under particular patterns or strengths of selection, and the possible disequilibrium sign patterns resulting from selection. These adult/viability results subsume those for populations with a gamete census and either constant fertility or viability selection. Although previous work suggests that the disequilibria generated by cytonuclear selection may be difficult to detect experimentally, this study shows that cytonuclear disequilibria at life stages with sex differences can be useful markers of the presence and strength of selection.     

Molecular phylogenetic approach for studying life-history evolution: the ambiguous example of the genus Medicago L

We present a molecular phylogeny including most species of the genus Medicago L. (Fabaceae). Based on the consensus of the 48 most parsimonious trees, life-history and mating-system characters are mapped, and a putative history of the genus is suggested. The most parsimonious reconstruction suggests an ancestral annual and selfing state, and recurrent evolution towards perenniality and outcrossing. Based on theoretical predictions and classical hypotheses of the history of the genus, different assumptions about the ancestral state and different weighting schemes of evolution between the character states are made. Assuming an outcrossing, perennial ancestral state (partly supported by morphological features) does not fundamentally change the reconstruction. To meet theoretical expectations, various weighting schemes favouring evolution towards annuality and selfing are applied. Influence and validity of such weighting schemes are discussed with regard to other studies.     

How should we explain variation in the genetic variance of traits?

Recent work has called attention to large differences among traits in the amount of standardized genetic variance they possess. There are four general factors which could play a role in causing this variation: mutation, elimination of deleterious variation, selection of favorable alleles, and balancing selection. Three factors could directly influence the mutational variability of traits: canalization, the mutational target size, and the timing of trait expression. Here I carry out simple tests of the importance of some of these factors using data from Drosophila melanogaster. I compiled information from the literature on the mutational and standing genetic variances in outbred populations, inferred the relative mutational target size of each trait, its a timing of expression, and used models of life history to calculate fitness sensitivities for each trait. Mutational variation seems to play an important role, as it is highly correlated with standing variance. The target size hypothesis was supported by a significant correlation between mutational variance and inferred target size. There was also a significant relationship between the timing of trait expression and mutational variance. These hypotheses are confounded by a correlation between timing and target size. The elimination and canalization hypotheses were not supported by these data, suggesting that they play a quantitatively less important role in determining overall variances. Additional information concerning the pleiotropic consequences of mutations would help to validate the fitness sensitivities used to test the elimination and canalization hypotheses.     

Effects of domestication on production and perception of mallard maternal alarm calls: Developmental lag in behavioral arousal.

Conducted field and laboratory studies to assess the effects of intense genetic selection on the production and perception of the maternal alarm calls of 150 domestic (Peking) and 120 wild mallard ducks (Anas platyrhynchos). With respect to production, the calls of wild and domestic Ss were comparable on 4 acoustic features and differed only slightly on 2 features. With respect to perception, the calls of wild and domestic hens were equally effective in promoting behavioral inhibition in wild and domestic ducklings. Although data reveal little or no effect of domestication on maternal alarm call, an unexpected effect was found regarding the domestic ducklings' behavior. Peking Ss showed a greater level of behavioral inhibition than mallards at 24 hrs of age. Further experiments indicated that the differential level of inhibition in the wild and domestic birds reflects a developmental lag in arousal consequent to domestication: 72-hr-old Peking ducklings were behaviorally more aroused than 24-hr-old Peking ducklings and were similar to 24-hr-old mallard ducklings in that respect. This appears to be the first demonstration of behavioral heterochrony, which is believed to be an important mechanism of behavioral evolution. (24 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Gulliver's further travels: the necessity and difficulty of a hierarchical theory of selection

For principled and substantially philosophical reasons, based largely on his reform of natural history by inverting the Paleyan notion of overarching and purposeful beneficence in the construction of organisms, Darwin built his theory of selection at the single causal level of individual bodies engaged in unconscious (and metaphorical) struggle for their own reproductive success. But the central logic of the theory allows selection to work effectively on entities at several levels of a genealogical hierarchy, provided that they embody a set of requisite features for defining evolutionary individuality. Genes, cell lineages, demes, species, and clades-as well as Darwin's favoured organisms-embody these requisite features in enough cases to form important levels of selection in the history of life. R. A. Fisher explicitly recognized the unassailable logic of species selection, but denied that thsi real process could be important in evolution because, compared with the production of new organisms within a species, the origin of new species is so rare, and the number of species within most clades so low. I review this and other classical arguments against higher-level selection, and conclude (in the first part of this paper) that they are invalid in practice for interdemic selection, and false in principle for species selection. Punctuated equilibrium defines the individuality of species and refutes Fisher's classical argument based on cycle time. In the second part of the paper, I argue that we have failed to appreciate the range and power of selection at levels above and below the organismic because we falsely extrapolate the defining properties of organisms to these other levels (which are characterized by quite different distinctive features), and then regard the other levels as impotent because their effective individuals differ so much from organisms. We would better appreciate the power and generality of hierarchical models of selection if we grasped two key principles: first, that levels can interact in all modes (positively, negatively, and orthogonally), and not only in the negative style (with a higher level suppressing an opposing force of selection from the lower level) that, for heuristic and operational reasons, has received almost exclusive attention in the existing literature; and second, that each hierarchical level differs from all others in substantial and interesting ways, both in the style and frequency of patterns in change and causal modes.     

Evolution, emotions, and emotional disorders.

Emotions research is now routinely grounded in evolution, but explicit evolutionary analyses of emotions remain rare. This article considers the implications of natural selection for several classic questions about emotions and emotional disorders. Emotions are special modes of operation shaped by natural selection. They adjust multiple response parameters in ways that have increased fitness in adaptively challenging situations that recurred over the course of evolution. They are valenced because selection shapes special processes for situations that have influenced fitness in the past. In situations that decrease fitness, negative emotions are useful and positive emotions are harmful. Selection has partially differentiated subtypes of emotions from generic precursor states to deal with specialized situations. This has resulted in untidy emotions that blur into each other on dozens of dimensions, rendering the quest for simple categorically distinct emotions futile. Selection has shaped flexible mechanisms that control the expression of emotions on the basis of an individual's appraisal of the meaning of events for his or her ability to reach personal goals. The prevalence of emotional disorders can be attributed to several evolutionary factors. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Measuring spontaneous deleterious mutation process

Parameters of the deleterious mutation process can be estimated using the data on genotypes, phenotypes, or fitnesses. These data can be on long-term evolution, on short-term changes, or on the properties of equilibrium populations. The two most important parameters at the genomic level, the total deleterious mutation rate U and the mutational pressure on fitness P, remain poorly known. Reliable data on the rates of presumably neutral evolution, together with less certain estimates of the functionally important fraction of the genome, suggest that in mammals U > 1. The magnitudes of inbreeding depression in populations of selfers imply U approximately 1 in flowering plants. The straightforward way to estimate P is to assay the decline of fitness in populations with relaxed selection. The relevant data are contradictory, possibly because the results of the measurement of fitness depend strongly on the environmental conditions.     

Stability and change of personality across the life course: The impact of age and major life events on mean-level and rank-order stability of the Big Five.

Does personality change across the entire life course, and are those changes due to intrinsic maturation or major life experiences? This longitudinal study investigated changes in the mean levels and rank order of the Big Five personality traits in a heterogeneous sample of 14,718 Germans across all of adulthood. Latent change and latent moderated regression models provided 4 main findings: First, age had a complex curvilinear influence on mean levels of personality. Second, the rank-order stability of Emotional Stability, Extraversion, Openness, and Agreeableness all followed an inverted U-shaped function, reaching a peak between the ages of 40 and 60 and decreasing afterward, whereas Conscientiousness showed a continuously increasing rank-order stability across adulthood. Third, personality predicted the occurrence of several objective major life events (selection effects) and changed in reaction to experiencing these events (socialization effects), suggesting that personality can change due to factors other than intrinsic maturation. Fourth, when events were clustered according to their valence, as is commonly done, effects of the environment on changes in personality were either overlooked or overgeneralized. In sum, our analyses show that personality changes throughout the life span, but with more pronounced changes in young and old ages, and that this change is partly attributable to social demands and experiences. (PsycINFO Database Record (c) 2011 APA, all rights reserved)     

Networks of gene regulation, neural development and the evolution of general capabilities, such as human empathy

A network of gene regulation organized in a hierarchical and combinatorial manner is crucially involved in the development of the neural network, and has to be considered one of the main substrates of genetic change in its evolution. Though qualitative features may emerge by way of the accumulation of rather unspecific quantitative changes, it is reasonable to assume that at least in some cases specific combinations of regulatory parts of the genome initiated new directions of evolution, leading to novel capabilities of the brain. These notions are applied, in this paper, to the evolution of the capability of cognition-based human empathy. It is suggested that it has evolved as a secondary effect of the evolution of strategic thought. Development of strategies depends on abstract representations of one's own possible future states in one's own brain to allow assessment of their emotional desirability, but also on the representation and emotional evaluation of possible states of others, allowing anticipation of their behaviour. This is best achieved if representations of others are connected to one's own emotional centres in a manner similar to self-representations. For this reason, the evolution of the human brain is assumed to have established representations with such linkages. No group selection is involved, because the quality of strategic thought affects the fitness of the individual. A secondary effect of this linkage is that both the actual states and the future perspectives of others elicit vicarious emotions, which may contribute to the motivations of altruistic behaviour.     

The cognitive differentiation-integration effort hypothesis: A synthesis between the fitness indicator and life history models of human intelligence.

This article presents a potential synthesis between the fitness indicator and life history models of human intelligence through consideration of the phenomena of ability differentiation and integration. The cognitive differentiation-integration effort hypothesis proposes that these effects result from a life history tradeoff between cognitive integration effort, a mating effort component associated with strengthening the positive manifold amongst abilities; and cognitive differentiation effort, a somatic effort component associated with the cultivation of specific abilities. This represents one of two largely independent sources of genetic variance in intelligence; the other is mediated by general fitness and mutation load and is associated with individual differences in levels of 'genetic g'. These two sources (along with a common source of environmental variance) combine to give rise to a variety of cognitive phenotypes characterized by different combinations of high or low levels of 'genetic g' and cognitive specialism or generalism. Fundamental to this model is the assumption that measures of life history speed (K) and g are essentially independent, which is demonstrated via meta-analysis of 10 studies reporting correlations between the variables (ρ = .023, ns, n = 2056). The implications of the model are discussed in an evolutionary, ecological, and developmental context. Seven key predictions are made in the discussion which if tested could provide definitive evidence for the hypothesis. (PsycINFO Database Record (c) 2011 APA, all rights reserved)     

Depletion of retinyl esters in the lungs coincides with lung prenatal morphological maturation

Close to birth rat fetuses have lungs which are depleted in retinyl esters. Glucocorticoids administered to pregnant rats accelerate this process. We have investigated changes in fetal lung levels of retinol and retinyl palmitate and accompanying morphological changes after administration of dexamethasone to pregnant rats on day 18 of pregnancy. Here we show that this depletion temporarily coincides with prenatal morphological maturation of the lungs. The data presented support the idea that the maturational effect of glucocorticoids in the developing lungs is linked to vitamin A metabolism.     

A fission-fusion origin for life

To develop a comprehensive 'cells-first' approach to the origin of life, we propose that protocells form spontaneously and that the fission and fusion of these protocells drives the dynamics of their evolution. The fitness criterion for this evolution is taken to be the the stability (conservation) of domains in the protocellular membrane as determined by non-covalent molecular associations between the amphiphiles of the membrane and a subset of the macromolecules in the protocell. In the presence of a source of free energy the macromolecular content of the protocell (co-)evolves as the result of (domain-dependent) membrane-catalysed polymerisation of the prebiotic constituents delivered to the protocell by fusion. The metabolism of the cell therefore (co-)evolves on a rugged fitness landscape. We indicate how domain evolution with the same fitness criterion can potentially give rise to coding. Membrane domains may therefore provide the link between protocells and the RNA/DNA-world.     

CaBPs and other immunohistochemical markers of the human vomeronasal system: a comparison with other mammals

After more than two centuries of almost sporadic inquiry as to the existence and function of the human vomeronasal system (VNS), the last decade has seen a resurgent interest in it. The principal question vexing many laboratories is whether adult humans retain the VNS that clearly develops during fetal growth. Additional questions are whether the structurally defined fetal VNS has any function role, and if this structure and function extend into postnatal life. One research tool that has been successfully used to identify key components of the mammalian VNS has been immunohistochemistry (IHC). This technique has clearly defined the vomeronasal receptor neurons in the vomeronasal organ, the vomeronasal nerve that projects into the central nervous system, and the target of this nerve, the accessory olfactory bulb. This review will discuss immunohistochemical studies that have identified these features in the mammalian VNS, and relate them to structural and IHC studies of the fetal and adult human VNS. Suggestions as to future studies to clarify the status of the human VNO also are offered.     

The evolutionary dynamics of selfish replicators: a two-level selection model

The aim of the present paper is to study the evolutionary dynamics of selfish replicators in a constant genetic background. Selfish replicators are viewed as alleles at a single locus, having a pleiotropic effect. Infinitely many alleles are possible; they act on individual fitness and have various levels of ability to distort segregation. This results in a two-level process of selection, including inter-individual selection (effect on individual fitness) and intra-individual selection (ability to distort segregation). The model takes other parameters into account, such as dominance, inbreeding and inbreeding depression. The system can have two different behaviours. (1) In some cases, evolutionary cycles are possible. The cycles correspond to an alternation of phases with predominant inter-individual selection, corresponding to major-effect mutations, and phases with predominant intra-individual selection, corresponding to small-effect mutations. (2) For other values of the parameters, a synthetic fitness can be defined: this absolute allelic fitness is estimated as a function of one's fitness due to both inter-individual and intra-individual selection. During the course of evolution, the synthetic fitness increases. The optimisation of a synthetic fitness is the most general process. The optimised value is essentially homologous to the value optimised for resource allocation to male and female function in hermaphrodites (female function being homologous to the effect on individual fitness, and male function being homologous to distortion ability). The relative importance of both behaviours is discussed. It is argued that repeated sequences causing some human degenerative hereditary diseases may follow a two-step evolutionary process: a progressive increase in number of sequences accompanied by a decrease of the individual fitness would be followed by massive elimination of such sequences. But in general the optimisation of the synthetic fitness seems to be more likely.     

The evolution of virus-induced apoptosis

Viruses from several different families are able to exploit their host's cell death programmes so as to maximize viral fitness. Consideration of the evolution of such strategies has lead to the suggestion that the virus should inhibit apoptosis, in order to prolong the life of the cell and thereby maximize the number of progeny virions. The host, on the other hand, should stimulate apoptosis thereby inhibiting viral growth and blocking viral spread. For example, the function of the latent membrane protein I (LMPI) of the Epstein-Barr virus and the bcl-2 homologue gene A179L of African swine fever virus is to inhibit apoptosis. However, in other cases it is the virus that stimulates cell death or the host that benefits from inhibiting apoptosis, such as in fatal alphavirus encephalitis. This has been explained by assuming that virus-induced apoptosis in non-regenerating cells would be detrimental to the host. We present a mathematical framework for understanding virus-induced apoptosis which accounts for these two opposite solutions to virus infection with respect to the mode of virus replication and the life cycle of the target cell.