Mothers in a cooperatively breeding bird increase investment per offspring at the pre-natal stage when they will have more help with post-natal care.

In many cooperative societies, including our own, helpers assist with the post-natal care of breeders' young and may thereby benefit the post-natal development of offspring. Here, we present evidence of a novel mechanism by which such post-natal helping could also have beneficial effects on pre-natal development: By lightening post-natal maternal workloads, helpers may allow mothers to increase their pre-natal investment per offspring. We present the findings of a decade-long study of cooperatively breeding white-browed sparrow-weaver, Plocepasser mahali, societies. Within each social group, reproduction is monopolized by a dominant breeding pair, and non-breeding helpers assist with nestling feeding. Using a within-mother reaction norm approach to formally identify maternal plasticity, we demonstrate that when mothers have more female helpers, they decrease their own post-natal investment per offspring (feed their nestlings at lower rates) but increase their pre-natal investment per offspring (lay larger eggs, which yield heavier hatchlings). That these plastic maternal responses are predicted by female helper number, and not male helper number, implicates the availability of post-natal helping per se as the likely driver (rather than correlated effects of group size), because female helpers feed nestlings at substantially higher rates than males. We term this novel maternal strategy "maternal front-loading" and hypothesize that the expected availability of post-natal help either allows or incentivizes helped mothers to focus maternal investment on the pre-natal phase, to which helpers cannot contribute directly. The potential for post-natal helping to promote pre-natal development further complicates attempts to identify and quantify the fitness consequences of helping.

Genetic and context-specific effects on individual inhibitory control performance in the guppy (Poecilia reticulata).

Among-individual variation in cognitive traits, widely assumed to have evolved under adaptive processes, is increasingly being demonstrated across animal taxa. As variation among individuals is required for natural selection, characterizing individual differences and their heritability is important to understand how cognitive traits evolve. Here, we use a quantitative genetic study of wild-type guppies repeatedly exposed to a 'detour task' to test for genetic variance in the cognitive trait of inhibitory control. We also test for genotype-by-environment interactions (GxE) by testing related fish under alternative experimental treatments (transparent vs. semi-transparent barrier in the detour-task). We find among-individual variation in detour task performance, consistent with differences in inhibitory control. However, analysis of GxE reveals that heritable factors only contribute to performance variation in one treatment. This suggests that the adaptive evolutionary potential of inhibitory control (and/or other latent variables contributing to task performance) may be highly sensitive to environmental conditions. The presence of GxE also implies that the plastic response of detour task performance to treatment environment is genetically variable. Our results are consistent with a scenario where variation in individual inhibitory control stems from complex interactions between heritable and plastic components.

Genetic improvement of speed across distance categories in thoroughbred racehorses in Great Britain.

Several studies over recent decades have reported a lack of contemporary improvement in thoroughbred racehorse speed, despite apparent additive genetic variance and putatively strong selection. More recently, it has been shown that some phenotypic improvement is ongoing, but rates are low in general and particularly so over longer distances. Here we used pedigree-based analysis of 692,534 records from 76,960 animals to determine whether these phenotypic trends are underpinned by genetic selection responses, and to evaluate the potential for more rapid improvement. We show that thoroughbred speed in Great Britain is only weakly heritable across sprint (h2 = 0.124), middle-distance (h2 = 0.122) and long-distance races (h2 = 0.074), but that mean predicted breeding values are nonetheless increasing across cohorts born between 1995 and 2012 (and racing from 1997 to 2014). For all three race distance categories, estimated rates of genetic improvement are statistically significant and also greater than can be explained by drift. Taken together our results show genetic improvement for thoroughbred speed is ongoing but slow, likely due to a combination of long generation times and low heritabilities. Additionally, estimates of realised selection intensities raises the possibility that the contemporary selection emerging from the collective actions of horse breeders is weaker than previously assumed, particularly over long distances. We suggest that unmodelled common environment effects may have upwardly biased estimates of heritability, and thus expected selection response, previously.

Differences in the temporal scale of reproductive investment across the slow-fast continuum in a passerine.

Life-history strategies differ with respect to investment in current versus 'future' reproduction, but when is this future? Under the novel 'temporality in reproductive investment hypothesis', we postulate variation should exist in the time frame over which reproductive costs are paid. Slow-paced individuals should pay reproductive costs over short (e.g. inter-annual) time scales to prevent reproductive costs accumulating, whereas fast-paced individuals should allow costs to accumulate (i.e. senescence). Using Fourier transforms, we quantify adjustments in clutch size with age, across four populations of blue tits (Cyanistes caeruleus). Fast populations had more prevalent and stronger long-term changes in reproductive investment, whereas slower populations had more prevalent short-term adjustments. Inter-annual environmental variation partly accounted for short-, but not long-term changes in reproductive investment. Our study reveals individuals differ in when they pay the cost of reproduction and that failure to partition this variation across different temporal scales and environments could underestimate reproductive trade-offs.

Sensory-based quantification of male colour patterns in Trinidadian guppies reveals no support for parallel phenotypic evolution in multivariate trait space.

Parallel evolution, in which independent populations evolve along similar phenotypic trajectories, offers insights into the repeatability of adaptive evolution. Here, we revisit a classic example of parallelism, that of repeated evolution of brighter males in the Trinidadian guppy (Poecilia reticulata). In guppies, colonisation of low predation habitats is associated with emergence of 'more colourful' phenotypes since predator-induced viability selection for crypsis weakens while sexual selection by female preference for conspicuousness remains strong. Our study differs from previous investigations in three respects. First, we adopted a multivariate phenotyping approach to characterise parallelism in multitrait space. Second, we used ecologically-relevant colour traits defined by the visual systems of the two selective agents (i.e., guppy, predatory cichlid). Third, we estimated population genetic structure to test for adaptive (parallel) evolution against a model of neutral phenotypic divergence. We find strong phenotypic differentiation that is inconsistent with a neutral model but very limited support for the predicted pattern of greater conspicuousness at low predation. Effects of predation regime on each trait were in the expected direction, but weak, largely nonsignificant, and explained little among-population variation. In multitrait space, phenotypic trajectories of lineages colonising low from high predation regimes were not parallel. Our results are consistent with reduced predation risk facilitating adaptive differentiation, potentially by female choice, but suggest that this proceeds in independent directions of multitrait space across lineages. Pool-sequencing data also revealed SNPs showing greater differentiation than expected under neutrality, among which some are found in genes contributing to colour pattern variation, presenting opportunities for future genetic study.

Partial sex linkage and linkage disequilibrium on the guppy sex chromosome.

The guppy Y chromosome has been considered a model system for the evolution of suppressed recombination between sex chromosomes, and it has been proposed that complete sex-linkage has evolved across about 3 Mb surrounding this fish's sex-determining locus, followed by recombination suppression across a further 7 Mb of the 23 Mb XY pair, forming younger "evolutionary strata". Sequences of the guppy genome show that Y is very similar to the X chromosome. Knowing which parts of the Y are completely nonrecombining, and whether there is indeed a large completely nonrecombining region, are important for understanding its evolution. Here, we describe analyses of PoolSeq data in samples from within multiple natural populations from Trinidad, yielding new results that support previous evidence for occasional recombination between the guppy Y and X. We detected recent demographic changes, notably that downstream populations have higher synonymous site diversity than upstream ones and other expected signals of bottlenecks. We detected evidence of associations between sequence variants and the sex-determining locus, rather than divergence under a complete lack of recombination. Although recombination is infrequent, it is frequent enough that associations with SNPs can suggest the region in which the sex-determining locus must be located. Diversity is elevated across a physically large region of the sex chromosome, conforming to predictions for a genome region with infrequent recombination that carries one or more sexually antagonistic polymorphisms. However, no consistently male-specific variants were found, supporting the suggestion that any completely sex-linked region may be very small.

Telomere length is highly heritable and independent of growth rate manipulated by temperature in field crickets.

Many organisms are capable of growing faster than they do. Restrained growth rate has functionally been explained by negative effects on lifespan of accelerated growth. However, the underlying mechanisms remain elusive. Telomere attrition has been proposed as a causal agent and has been mostly studied in endothermic vertebrates. We established that telomeres exist as chromosomal-ends in a model insect, the field cricket Gryllus campestris, using terminal restriction fragment and Bal 31 methods. Telomeres comprised TTAGGn repeats of 38 kb on average, more than four times longer than the telomeres of human infants. Bal 31 assays confirmed that telomeric repeats were located at the chromosome-ends. We tested whether rapid growth between day 1, day 65, day 85, and day 125 is achieved at the expense of telomere length by comparing nymphs reared at 23°C with their siblings reared at 28°C, which grew three times faster in the initial 65 days. Surprisingly, neither temperature treatment nor age affected average telomere length. Concomitantly, the broad sense heritability of telomere length was remarkably high at ~100%. Despite high heritability, the evolvability (a mean-standardized measure of genetic variance) was low relative to that of body mass. We discuss our findings in the context of telomere evolution. Some important features of vertebrate telomere biology are evident in an insect species dating back to the Triassic. The apparent lack of an effect of growth rate on telomere length is puzzling, suggesting strong telomere length maintenance during the growth phase. Whether such maintenance of telomere length is adaptive remains elusive and requires further study investigating the links with fitness in the wild.

Genetic and social contributions to sex differences in lifespan in Drosophila serrata.

Sex differences in lifespan remain an intriguing puzzle in evolutionary biology. While explanations range from sex differences in selection to sex differences in the expression of recessive lifespan-altering mutations (via X-linkage), little consensus has been reached. One unresolved issue is the extent to which genetic influences on lifespan dimorphism are modulated by the environment. For example, studies have shown that sex differences in lifespan can either increase or decrease depending upon the social environment. Here, we took an experimental approach, manipulating multiple axes of the social environment across inbred long- and short-lived genotypes and their reciprocal F1s in the fly Drosophila serrata. Our results reveal strong genetic effects and subtle yet significant genotype-by-environment interactions for male and female lifespan, specifically due to both population density and mating status. Further, our data do not support the idea that unconditional expression of deleterious X-linked recessive alleles in heterogametic males accounts for lower male lifespan.

Bacterial dispersal and drift drive microbiome diversity patterns within a population of feral hindgut fermenters.

Studies of microbiome variation in wildlife often emphasize host physiology and diet as proximate selective pressures acting on host-associated microbiota. In contrast, microbial dispersal and ecological drift are more rarely considered. Using amplicon sequencing, we characterized the bacterial microbiome of adult female (n = 86) Sable Island horses (Nova Scotia, Canada) as part of a detailed individual-based study of this feral population. Using data on sampling date, horse location, age, parental status, and local habitat variables, we contrasted the ability of spatiotemporal, life history, and environmental factors to explain microbiome diversity among Sable Island horses. We extended inferences made from these analyses with both phylogeny-informed and phylogeny-independent null modelling approaches to identify deviations from stochastic expectations. Phylogeny-informed diversity measures were correlated with spatial and local habitat variables, but null modelling results suggested that heterogeneity in ecological drift, rather than differential selective pressures acting on the microbiome, was responsible for these correlations. Conversely, phylogeny-independent diversity measures were best explained by host spatial and social structure, suggesting that taxonomic composition of the microbiome was shaped most strongly by bacterial dispersal. Parental status was important but correlated with measures of ß-dispersion rather than ß-diversity (mares without foals had lower alpha diversity and more variable microbiomes than mares with foals). Our results suggest that between host microbiome variation within the Sable Island horse population is driven more strongly by bacterial dispersal and ecological drift than by differential selective pressures. These results emphasize the need to consider alternative ecological processes in the study of microbiomes.

Genetic, social and maternal contributions to Mycobacterium bovis infection status in European badgers (Meles meles).

Within host populations, individuals can vary in their susceptibility to infections and in the severity and progression of disease once infected. Though mediated through differences in behaviour, resistance or tolerance, variation in disease outcomes ultimately stems from genetic and environmental (including social) factors. Despite obvious implications for the evolutionary, ecological and epidemiological dynamics of disease traits, the relative importance of these factors has rarely been quantified in naturally infected wild animal hosts. Here, we use a long-term capture-mark-recapture study of group-living European badgers (Meles meles) to characterize genetic and environmental sources of variation in host infection status by Mycobacterium bovis, the causative agent of bovine tuberculosis (bTB). We find that genetic factors contribute to M. bovis infection status, whether measured over a lifetime or across repeated captures. In the latter case, the heritability (h2 ) of infection status is close to zero in cubs and yearlings but increases in adulthood. Overall, environmental influences arising from a combination of social group membership (defined in time and space) and maternal effects appear to be more important than genetic factors. Thus, while genes do contribute to among-individual variation, they play a comparatively minor role, meaning that rapid evolution of host defences under parasite-mediated selection is unlikely (especially if selection is on young animals where h2 is lowest). Conversely, our results lend further support to the view that social and early-life environments are important drivers of the dynamics of bTB infection in badger populations specifically, and of disease traits in wild hosts more generally.

Efficacy and safety of minimally invasive surgery with thrombolysis in intracerebral haemorrhage evacuation (MISTIE III): a randomised, controlled, open-label, blinded endpoint phase 3 trial.

BACKGROUND: Acute stroke due to supratentorial intracerebral haemorrhage is associated with high morbidity and mortality. Open craniotomy haematoma evacuation has not been found to have any benefit in large randomised trials. We assessed whether minimally invasive catheter evacuation followed by thrombolysis (MISTIE), with the aim of decreasing clot size to 15 mL or less, would improve functional outcome in patients with intracerebral haemorrhage. METHODS: MISTIE III was an open-label, blinded endpoint, phase 3 trial done at 78 hospitals in the USA, Canada, Europe, Australia, and Asia. We enrolled patients aged 18 years or older with spontaneous, non-traumatic, supratentorial intracerebral haemorrhage of 30 mL or more. We used a computer-generated number sequence with a block size of four or six to centrally randomise patients to image-guided MISTIE treatment (1·0 mg alteplase every 8 h for up to nine doses) or standard medical care. Primary outcome was good functional outcome, defined as the proportion of patients who achieved a modified Rankin Scale (mRS) score of 0-3 at 365 days, adjusted for group differences in prespecified baseline covariates (stability intracerebral haemorrhage size, age, Glasgow Coma Scale, stability intraventricular haemorrhage size, and clot location). Analysis of the primary efficacy outcome was done in the modified intention-to-treat (mITT) population, which included all eligible, randomly assigned patients who were exposed to treatment. All randomly assigned patients were included in the safety analysis. This study is registered with ClinicalTrials.gov, number NCT01827046. FINDINGS: Between Dec 30, 2013, and Aug 15, 2017, 506 patients were randomly allocated: 255 (50%) to the MISTIE group and 251 (50%) to standard medical care. 499 patients (n=250 in the MISTIE group; n=249 in the standard medical care group) received treatment and were included in the mITT analysis set. The mITT primary adjusted efficacy analysis estimated that 45% of patients in the MISTIE group and 41% patients in the standard medical care group had achieved an mRS score of 0-3 at 365 days (adjusted risk difference 4% [95% CI -4 to 12]; p=0·33). Sensitivity analyses of 365-day mRS using generalised ordered logistic regression models adjusted for baseline variables showed that the estimated odds ratios comparing MISTIE with standard medical care for mRS scores higher than 5 versus 5 or less, higher than 4 versus 4 or less, higher than 3 versus 3 or less, and higher than 2 versus 2 or less were 0·60 (p=0·03), 0·84 (p=0·42), 0·87 (p=0·49), and 0·82 (p=0·44), respectively. At 7 days, two (1%) of 255 patients in the MISTIE group and ten (4%) of 251 patients in the standard medical care group had died (p=0·02) and at 30 days, 24 (9%) patients in the MISTIE group and 37 (15%) patients in the standard medical care group had died (p=0·07). The number of patients with symptomatic bleeding and brain bacterial infections was similar between the MISTIE and standard medical care groups (six [2%] of 255 patients vs three [1%] of 251 patients; p=0·33 for symptomatic bleeding; two [1%] of 255 patients vs 0 [0%] of 251 patients; p=0·16 for brain bacterial infections). At 30 days, 76 (30%) of 255 patients in the MISTIE group and 84 (33%) of 251 patients in the standard medical care group had one or more serious adverse event, and the difference in number of serious adverse events between the groups was statistically significant (p=0·012). INTERPRETATION: For moderate to large intracerebral haemorrhage, MISTIE did not improve the proportion of patients who achieved a good response 365 days after intracerebral haemorrhage. The procedure was safely adopted by our sample of surgeons. FUNDING: National Institute of Neurological Disorders and Stroke and Genentech.

Genetic variance for behavioural 'predictability' of stress response.

Genetic factors underpinning phenotypic variation are required if natural selection is to result in adaptive evolution. However, evolutionary and behavioural ecologists typically focus on variation among individuals in their average trait values and seek to characterize genetic contributions to this. As a result, less attention has been paid to if and how genes could contribute towards within-individual variance or trait 'predictability'. In fact, phenotypic 'predictability' can vary among individuals, and emerging evidence from livestock genetics suggests this can be due to genetic factors. Here, we test this empirically using repeated measures of a behavioural stress response trait in a pedigreed population of wild-type guppies. We ask (a) whether individuals differ in behavioural predictability and (b) whether this variation is heritable and so evolvable under selection. Using statistical methodology from the field of quantitative genetics, we find support for both hypotheses and also show evidence of a genetic correlation structure between the behavioural trait mean and individual predictability. We show that investigating sources of variability in trait predictability is statistically tractable and can yield useful biological interpretation. We conclude that, if widespread, genetic variance for 'predictability' will have major implications for the evolutionary causes and consequences of phenotypic variation.

Choice consequences: salinity preferences and hatchling survival in the mangrove rivulus (Kryptolebias marmoratus).

In heterogeneous environments, mobile species should occupy habitats in which their fitness is maximized. Mangrove rivulus fish inhabit mangrove ecosystems where salinities range from 0 to 65 ppt, but are most often collected from areas with salinities of ∼25 ppt. We examined the salinity preference of mangrove rivulus in a lateral salinity gradient, in the absence of predators and competitors. Fish could swim freely for 8 h throughout the gradient with chambers containing salinities ranging from 5 to 45 ppt (or 25 ppt throughout in the control). We defined preference as the salinity in which the fish spent most of their time, and also measured preference strength, latency to begin exploring the arena, and number of transitions between chambers. To determine whether these traits were repeatable, each fish experienced three trials. Mangrove rivulus spent a greater proportion of time in salinities lower (5-15 ppt) than they occupy in the wild. Significant among-individual variation in the (multivariate) behavioral phenotype emerged when animals experienced the gradient, indicating strong potential for selection to drive behavioral evolution in areas with diverse salinity microhabitats. We also showed that mangrove rivulus had a significantly greater probability of laying eggs in low salinities compared with control or high salinities. Eggs laid in lower salinities also had higher hatching success compared with those laid in higher salinities. Thus, although mangrove rivulus can tolerate a wide range of salinities, they prefer low salinities. These results raise questions about factors that prevent mangrove rivulus from occupying lower salinities in the wild, whether higher salinities impose energetic costs, and whether fitness changes as a function of salinity.

End-tidal and arterial carbon dioxide gradient in serious traumatic brain injury after prehospital emergency anaesthesia: a retrospective observational study.

OBJECTIVES: In the UK, 20% of patients with severe traumatic brain injury (TBI) receive prehospital emergency anaesthesia (PHEA). Current guidance recommends an end-tidal carbon dioxide (ETCO2) of 4.0-4.5 kPa (30.0-33.8 mm Hg) to achieve a low-normal arterial partial pressure of CO2 (PaCO2), and reduce secondary brain injury. This recommendation assumes a 0.5 kPa (3.8 mm Hg) ETCO2-PaCO2 gradient. However, the gradient in the acute phase of TBI is unknown. The primary aim was to report the ETCO2-PaCO2 gradient of TBI patients at hospital arrival. METHODS: A retrospective cohort study of adult patients with serious TBI, who received a PHEA by a prehospital critical care team in the East of England between 1 April 2015 and 31 December 2017. Linear regression was performed to test for correlation and reported as R-squared (R2). A Bland-Altman plot was used to test for paired ETCO2 and PaCO2 agreement and reported with 95% CI. ETCO2-PaCO2 gradient data were compared with a two-tailed, unpaired, t-test. RESULTS: 107 patients were eligible for inclusion. Sixty-seven patients did not receive a PaCO2 sample within 30 min of hospital arrival and were therefore excluded. Forty patients had complete data and were included in the final analysis; per protocol. The mean ETCO2-PaCO2 gradient was 1.7 (±1.0) kPa (12.8 mm Hg), with moderate correlation (R2=0.23, p=0.002). The Bland-Altman bias was 1.7 (95% CI 1.4 to 2.0) kPa with upper and lower limits of agreement of 3.6 (95% CI 3.0 to 4.1) kPa and -0.2 (95% CI -0.8 to 0.3) kPa, respectively. There was no evidence of a larger gradient in more severe TBI (p=0.29). There was no significant gradient correlation in patients with a coexisting serious thoracic injury (R2=0.13, p=0.10), and this cohort had a larger ETCO2-PaCO2 gradient, 2.0 (±1.1) kPa (15.1 mm Hg), p=0.01. Patients who underwent prehospital arterial blood sampling had an arrival PaCO2 of 4.7 (±0.2) kPa (35.1 mm Hg). CONCLUSION: There is only moderate correlation of ETCO2 and PaCO2 at hospital arrival in patients with serious TBI. The mean ETCO2-PaCO2 gradient was 1.7 (±1.0) kPa (12.8 mm Hg). Lower ETCO2 targets than previously recommended may be safe and appropriate, and there may be a role for prehospital PaCO2 measurement.

Ejaculate-mediated paternal effects: evidence, mechanisms and evolutionary implications.

Despite serving the primary objective of ensuring that at least one sperm cell reaches and fertilises an ovum, the male ejaculate (i.e. spermatozoa and seminal fluid) is a compositionally complex 'trait' that can respond phenotypically to subtle changes in conditions. In particular, recent research has shown that environmentally and genetically induced changes to ejaculates can have implications for offspring traits that are independent of the DNA sequence encoded into the sperm's haploid genome. In this review, we compile evidence from several disciplines and numerous taxonomic systems to reveal the extent of such ejaculate-mediated paternal effects (EMPEs). We consider a number of environmental and genetic factors that have been shown to impact offspring phenotypes via ejaculates, and where possible, we highlight the putative mechanistic pathways by which ejaculates can act as conduits for paternal effects. We also highlight how females themselves can influence EMPEs, and in some cases, how maternally derived sources of variance may confound attempts to test for EMPEs. Finally, we consider a range of putative evolutionary implications of EMPEs and suggest a number of potentially useful approaches for exploring these further. Overall, our review confirms that EMPEs are both widespread and varied in their effects, although studies reporting their evolutionary effects are still in their infancy.

Social effects of territorial neighbours on the timing of spring breeding in North American red squirrels.

Organisms can affect one another's phenotypes when they socially interact. Indirect genetic effects occur when an individual's phenotype is affected by genes expressed in another individual. These heritable effects can enhance or reduce adaptive potential, thereby accelerating or reversing evolutionary change. Quantifying these social effects is therefore crucial for our understanding of evolution, yet estimates of indirect genetic effects in wild animals are limited to dyadic interactions. We estimated indirect phenotypic and genetic effects, and their covariance with direct effects, for the date of spring breeding in North American red squirrels (Tamiasciurus hudsonicus) living in an array of territories of varying spatial proximity. Additionally, we estimated indirect effects and the strength of selection at low and high population densities. Social effects of neighbours on the date of spring breeding were different from zero at high population densities but not at low population densities. Indirect phenotypic effects accounted for a larger amount of variation in the date of breeding than differences attributable to the among-individual variance, suggesting social interactions are important for determining breeding dates. The genetic component to these indirect effects was however not statistically significant. We therefore showcase a powerful and flexible method that will allow researchers working in organisms with a range of social systems to estimate indirect phenotypic and genetic effects, and demonstrate the degree to which social interactions can influence phenotypes, even in a solitary species.

Evolutionary genetics of personality in the Trinidadian guppy I: maternal and additive genetic effects across ontogeny.

Among-individual variation in behaviour is a widespread phenomenon, with several frameworks developed to explain its existence. Maternal effects, which can have significant influence over evolutionary processes, are an understudied source of behavioural variation. Maternal effects are not necessarily static, however, since their importance can change over offspring ontogeny, typically declining with age relative to additive genetic effects. Here, using a quantitative genetics approach, we test the prediction that maternal effects will influence age-specific risk-taking behaviour in Trinidadian guppies, Poecilia reticulata. Individuals were subject to a single open-field trial as juveniles and up to four repeat trials as adults, with five traits indicative of risk-taking behaviour measured in each trial. We then partitioned phenotypic variance into additive genetic (VA) and maternal identity (VM) components, in addition to testing brood size and maternal weight as specific sources of maternal effects. We found that VM had significant influence over juvenile traits, with very low VA estimates. Whereas, in adults, all traits were significantly heritable, with little support for VM. We also found a strong influence of maternal traits on juvenile behaviours as predicted, with significant, albeit smaller, effects found in adults. Maternal weight was heritable and itself subject to maternal effects. Thus, maternal weight is a likely source of maternal genetic effects that are expected to alter response to selection on personality in this system. More generally, our study highlights that while maternal effects can be an important source of personality variation, this varies over ontogeny of offspring.

Evolutionary genetics of personality in the Trinidadian guppy II: sexual dimorphism and genotype-by-sex interactions.

Sexual dimorphism in behaviour and personality has been identified in a number of species, but few studies have assessed the extent of shared genetic architecture across the sexes. Under sexually antagonistic selection, mechanisms are expected to evolve that reduce evolutionary conflict, resulting in genotype-by-sex (GxS) interactions. Here we assess the extent of sexual dimorphism in four risk-taking behaviour traits in the Trinidadian guppy, Poecilia reticulata, and apply a multivariate approach to test for GxS interactions. We also quantify the among-individual and genetic covariances between personality and size and growth, which are known a priori to differ between the sexes. We found significant sexual dimorphism in three of the four behaviours, although rmf between sex-specific homologous traits was significantly <+1 for only one behaviour. Using multivariate models, we then estimated sex-specific genetic (co)variance matrices (Gm and Gf) and tested for asymmetry of the cross-trait cross-sex genetic covariance structure (submatrix B). While Gm and Gf were not significantly different from each other overall, their respective leading eigenvectors were poorly aligned. Statistical support for asymmetry in B was found, but limited to a single trait pair for which the cross-sex covariances differed (i.e., COVA(m,f) ≠ COVA(f,m)). Thus, while single- and multi-trait perspectives evidence some GxS, the overall picture is one of similarity between the sexes in their genetic (co)variance structures. Our results suggest behavioural traits related to risk-taking may lack the sex-specific genetic architecture for further dimorphism to evolve under what is hypothesised to be antagonistic selection.

Correction: Development of G: a test in an amphibious fish.

Figure 3 legend has been corrected to state: "Difference matrices for pairwise-trait phenotypic correlations (rP, below diagonal) and pairwise-trait genetic correlations (rG, above diagonal) from 1, 15, and 100 DPH. Differences are color coded by strength and direction. Differences shown in gray are positive and differences shown in black are negative. When ages are similar, the colored square is small; when ages are very different, the colored square fills the cell. EPL Epural length, EPA epural angle, PHPL parahypural length, PHPA parahypural angle, HYPL hypural length, HYPW hypural width, and SL standard length."

Development of G: a test in an amphibious fish.

Heritable variation in, and genetic correlations among, traits determine the response of multivariate phenotypes to natural selection. However, as traits develop over ontogeny, patterns of genetic (co)variation and integration captured by the G matrix may also change. Despite this, few studies have investigated how genetic parameters underpinning multivariate phenotypes change as animals pass through major life history stages. Here, using a self-fertilizing hermaphroditic fish species, mangrove rivulus (Kryptolebias marmoratus), we test the hypothesis that G changes from hatching through reproductive maturation. We also test Cheverud's conjecture by asking whether phenotypic patterns provide an acceptable surrogate for patterns of genetic (co)variation within and across ontogenetic stages. For a set of morphological traits linked to locomotor (jumping) performance, we find that the overall level of genetic integration (as measured by the mean-squared correlation across all traits) does not change significantly over ontogeny. However, we also find evidence that some trait-specific genetic variances and pairwise genetic correlations do change. Ontogenetic changes in G indicate the presence of genetic variance for developmental processes themselves, while also suggesting that any genetic constraints on morphological evolution may be age-dependent. Phenotypic correlations closely resembled genetic correlations at each stage in ontogeny. Thus, our results are consistent with the premise that-at least under common environment conditions-phenotypic correlations can be a good substitute for genetic correlations in studies of multivariate developmental evolution.