Project description:BackgroundSince Darwin's pioneering work, evolutionary changes in isolated island populations of vertebrates have continued to provide the strongest evidence for the theory of natural selection. Besides macro-evolutionary changes, micro-evolutionary changes and the relative importance of natural selection vs. genetic drift are under intense investigation. Our study focuses on the genetic differentiation in morphological and life-history traits in insular populations of a small mammal the bank vole Myodes glareolus.ResultsOur results do not support the earlier findings for larger adult size or lower reproductive effort in insular populations of small mammals. However, the individuals living on islands produced larger offspring than individuals living on the mainland. Genetic differentiation in offspring size was further confirmed by the analyses of quantitative genetics in lab. In insular populations, genetic differentiation in offspring size simultaneously decreases the additive genetic variation (VA) for that trait. Furthermore, our analyses of differentiation in neutral marker loci (Fst) indicate that VA is less than expected on the basis of genetic drift alone, and thus, a lower VA in insular populations could be caused by natural selection.ConclusionWe believe that different selection pressures (e.g. higher intraspecific competition) in an insular environment might favour larger offspring size in small mammals. Island selection for larger offspring could be the preliminary mechanism in a process which could eventually lead to a smaller litter size and lower reproductive effort frequently found in insular vertebrates.
Project description:Plasma lipid levels are highly heritable traits, but known genetic loci can only explain a small portion of their heritability. In this study, we analyzed the role of parental levels of total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), and triglycerides (TGs) in explaining the values of the corresponding traits in adult offspring. We also evaluated the contribution of nongenetic factors that influence lipid traits (age, body mass index, smoking, medications, and menopause) alone and in combination with variability at the genetic loci known to associate with TC, LDL-C, HDL-C, and TG levels. We performed comparisons among different sex-specific regression models in 416 families from the Framingham Heart Study and 304 from the SardiNIA cohort. Models including parental lipid levels explain significantly more of the trait variation than models without these measures, explaining up to ≈39% of the total trait variation. Of this variation, the parent-of-origin effect explains as much as ≈15% and it does so in a sex-specific way. This observation is not owing to shared environment, given that spouse-pair correlations were negligible (<1.5% explained variation in all cases) and is distinct from previous genetic and acquired factors that are known to influence serum lipid levels. These findings support the concept that unknown genetic and epigenetic contributors are responsible for most of the heritable component of the plasma lipid phenotype, and that, at present, the clinical utility of knowing age-matched parental lipid levels in assessing risk of dyslipidemia supersedes individual locus effects. Our results support the clinical utility of knowing parental lipid levels in assessing future risk of dyslipidemia.
Project description:The age at which a parent has a child impacts the child's cognition and risk for mental illness. It appears that this risk is curvilinear, with both age extremes associated with lower intelligence and increased prevalence of some neuropsychiatric disorders. Little is known of the neural mechanisms underpinning this phenomenon. We extracted lobar volumes, surface areas, and cortical thickness from 489 neuroanatomic magnetic resonance images acquired on 171 youth. Using linear mixed model regression, we determined the association between parental age and offspring's neuroanatomy, adjusting for offspring's age, sex, intelligence, and parental socioeconomic class. For gray matter volumes, quadratic paternal and maternal age terms contributed significantly (maternal quadratic age effect: t = -2.2, P = 0.03; paternal quadratic age effect: t = -2.4, P = 0.02) delineating an inverted "U" relationship between parental age and gray matter volume. Cortical volume increased with both advancing paternal and maternal age until around the early 30s after which it fell. Paternal age effects were more pronounced on cortical surface area, whereas maternal age impacted more on cortical thickness. There were no significant effects of parental age on white matter volumes. These parental age effects on cerebral morphology may form part of the link between parental age extremes and suboptimal neurocognitive outcomes.
Project description:Because egg-laying meant that even the largest dinosaurs gave birth to very small offspring, they had to pass through multiple ontogenetic life stages to adulthood. Dinosaurs' successors as the dominant terrestrial vertebrate life form, the mammals, give birth to live young, and have much larger offspring and less complex ontogenetic histories. The larger number of juveniles in dinosaur as compared to mammal ecosystems represents both a greater diversity of food available to predators, and competitors for similar-sized individuals of sympatric species. Models of population abundances across different-sized species of dinosaurs and mammals, based on simulated ecological life tables, are employed to investigate how differences in predation and competition pressure influenced dinosaur communities. Higher small- to medium-sized prey availability leads to a normal body mass-species richness (M-S) distribution of carnivorous dinosaurs (as found in the theropod fossil record), in contrast to the right-skewed M-S distribution of carnivorous mammals (as found living members of the order Carnivora). Higher levels of interspecific competition leads to a left-skewed M-S distribution in herbivorous dinosaurs (as found in sauropods and ornithopods), in contrast to the normal M-S distribution of large herbivorous mammals. Thus, our models suggest that differences in reproductive strategy, and consequently ontogeny, explain observed differences in community structure between dinosaur and mammal faunas. Models also show that the largest dinosaurian predators could have subsisted on similar-sized prey by including younger life stages of the largest herbivore species, but that large predators likely avoided prey much smaller than themselves because, despite predicted higher abundances of smaller than larger-bodied prey, contributions of small prey to biomass intake would be insufficient to satisfy meat requirements. A lack of large carnivores feeding on small prey exists in mammals larger than 21.5 kg, and it seems a similar minimum prey-size threshold could have affected dinosaurs as well.
Project description:We examine the influences of a set of early life conditions (ELCs) on all-cause and cause-specific mortality among elderly individuals, with special attention to one of the most dramatic early events in a child's, adolescent's, or even young adult's life, the death of a parent. The foremost question is, once controlling for prevailing (and potentially confounding) conditions early in life (family history of longevity, paternal characteristics (SES, age at time of birth, sibship size, and religious affiliation)), is a parental death associated with enduring mortality risks after age 65? The years following parental death may initiate new circumstances through which the adverse effects of paternal death operate. Here we consider the offspring's marital status (whether married; whether and when widowed), adult socioeconomic status, fertility, and later life health status. Adult health status is based on the Charlson Co-Morbidity Index, a construct that summarizes nearly all serious illnesses afflicting older individuals that relies on Medicare data. The data are based on linkages between the Utah Population Database and Medicare claims that hold medical diagnoses data. We show that offspring whose parents died when they were children, but especially when they were adolescents/young adults, have modest but significant mortality risks after age 65. What are striking are the weak mediating influences of later-life comorbidities, marital status, fertility and adult socioeconomic status since controls for these do little to alter the overall association. No beneficial effects of the surviving parent's remarriage were detected. Overall, we show the persistence of the effects of early life loss on later-life mortality and indicate the difficulties in addressing challenges at young ages.
Project description:Old parental age is commonly associated with negative effects on offspring life-history traits. Such parental senescence effects are predicted to have a cumulative detrimental effect over successive generations. However, old parents may benefit from producing higher quality offspring when these compete for seasonal resources. Thus, old parents may choose to increase investment in their offspring, thereby producing fewer but larger and more competitive progeny. We show that Caenorhabditis elegans hermaphrodites increase parental investment with advancing age, resulting in fitter offspring who reach their reproductive peak earlier. Remarkably, these effects increased over six successive generations of breeding from old parents and were subsequently reversed following a single generation of breeding from a young parent. Our findings support the hypothesis that offspring of old parents receive more resources and convert them into increasingly faster life histories. These results contradict the theory that old parents transfer a cumulative detrimental 'ageing factor' to their offspring.
Project description:Parents adjust their reproductive investment over their lifespan based on their condition, age, and social environment, creating the potential for inter-generational effects to differentially affect offspring physiology. To date, however, little is known about how social environments experienced by parents throughout development and adulthood influence the effect of parental age on the expression of life-history traits in the offspring. Here, I collected data on Drosophila melanogaster offspring traits (i.e., body weight, water content, and lipid reserves) from populations where either mothers, fathers both, or neither parents experienced different social environments during development (larval crowding) and adulthood. Parental treatment modulated parental age effects on offspring lipid reserves but did not influence parental age effects on offspring water content. Importantly, parents in social environments where all individuals were raised in uncrowded larval densities produced daughters and sons lighter than parental treatments which produced the heaviest offspring. The peak in offspring body weight was delayed relative to the peak in parental reproductive success, but more strongly so for daughters from parental treatments where some or all males in the parental social environments were raised in crowded larval densities (irrespective of their social context), suggesting a potential father-to-daughter effect. Overall, the findings of this study reveal that parental ecological history (here, developmental and adult social environments) can modulate the effects of parental age at reproduction on the expression of offspring traits.
Project description:While there is evidence that longevity runs in families, the study of long-lived families is complicated by the fact that longevity-related information is available only for the oldest old, many of whom may be deceased and unavailable for testing, and information on other living family members, primarily descendents, is censored. This situation requires a creative approach for analyzing determinants of longevity in families. There are likely biomarkers that predict an individual's longevity, suggesting the possibility that those biomarkers which are heritable may constitute valuable endophenotypes for exceptional survival. These endophenotypes could be studied in families to identify human longevity genes and elucidate possible mechanisms of their influence on longevity. In this paper, we analyze data collected in the Long Life Family Study (LLFS) investigating whether indicators of physiological state, cognitive functioning and health/well-being among offspring predict longevity in parents. Good predictors can be used as endophenotypes for exceptional survival. Our analyses revealed significant associations between cumulative indices describing physiological state, as well as a number of offspring phenotypes, and parental lifespan, supporting both their familial basis and relevance to longevity. We conclude that the study of endophenotypes within families is a valid approach to the genetics of human longevity.
Project description:It is a long-standing challenge to understand how changes in food resources impact consumer life history traits and, in turn, impact how organisms interact with their environment. To characterize food quality effects on life history, most studies follow organisms throughout their life cycle and quantify major life events, such as age at maturity or fecundity. From these studies, we know that food quality generally impacts body size, juvenile development, and life span. Importantly, throughout juvenile development, many organisms develop through several stages of growth that can have different interactions with their environment. For example, some parasitoids typically attack larger instars, whereas larval insect predators typically attack smaller instars. Interestingly, most studies lump all juvenile stages together, which ignores these ecological changes over juvenile development.We combine a cross-sectional experimental approach with a stage-structured population model to estimate instar-specific vital rates in the bean weevil, Callosobruchus maculatus across a food quality gradient. We characterize food quality effects on the bean weevil's life history traits throughout its juvenile ontogeny to test how food quality impacts instar-specific vital rates.Vital rates differed across food quality treatments within each instar; however, their effect differed with instar. Weevils consuming low-quality food spent 38%, 37%, and 18% more time, and were 34%, 53%, and 63% smaller than weevils consuming high-quality food in the second, third, and fourth instars, respectively. Overall, our results show that consuming poor food quality means slower growth, but that food quality effects on vital rates, growth and development are not equal across instars. Differences in life history traits over juvenile ontogeny in response to food quality may impact how organisms interact with their environment, including how susceptible they are to predation, parasitism, and their competitive ability.
Project description:It has recently been proposed that life-history evolution is subject to a fundamental size-dependent constraint. This constraint limits the rate at which biomass can be produced so that production per unit of body mass is inevitably slower in larger organisms than in smaller ones. Here we derive predictions for how changes in body size and production rates evolve in different lifestyles subject to this constraint. Predictions are tested by using data on the mass of neonate tissue produced per adult per year in 637 placental mammal species and are generally supported. Compared with terrestrial insectivores with generalized primitive traits, mammals that have evolved more specialized lifestyles have divergent mass-specific production rates: (i) increased in groups that specialize on abundant and reliable foods: grazing and browsing herbivores (artiodactyls, lagomorphs, perissodactyls, and folivorous rodents) and flesh-eating marine mammals (pinnipeds, cetaceans); and (ii) decreased in groups that have lifestyles with reduced death rates: bats, primates, arboreal, fossorial, and desert rodents, bears, elephants, and rhinos. Convergent evolution of groups with similar lifestyles is common, so patterns of productivity across mammalian taxa reflect both ecology and phylogeny. The overall result is that groups with different lifestyles have parallel but offset relationships between production rate and body size. These results shed light on the evolution of the fast-slow life-history continuum, suggesting that variation occurs along two axes corresponding to body size and lifestyle.