Genetic influences on growth traits of BMI: a longitudinal study of adult twins

Objective: To investigate the interplay between genetic factors influencing baseline level and changes in BMI in adulthood. Methods and Procedures: A longitudinal twin study of the cohort of Finnish twins (N = 10,556 twin individuals) aged 20–46 years at baseline was conducted and followed up 15 years. Data on weight and height were obtained from mailed surveys in 1975, 1981, and 1990. Results: Latent growth models revealed a substantial genetic influence on BMI level at baseline in males and females (heritability (h²) 80% (95% confidence interval 0.79–0.80) for males and h² = 82% (0.81, 0.84) for females) and a moderate‐to‐high influence on rate of change in BMI (h² = 58% (0.50, 0.69) for males and h² = 64% (0.58, 0.69) for females). Only very weak evidence for genetic pleiotropy was observed; the genetic correlation between baseline and rate of change in BMI was very modest (−0.070 (–0.13, −0.068) for males and 0.04 (0.00, 0.08) for females. Discussion: Our population‐based results provide a basis for identifying genetic variants for change in BMI, in particular weight gain. Furthermore, they demonstrate for the first time that such genetic variants for change in BMI are likely to be different from those affecting level of BMI.     

Familial Resemblance of 7‐Year Changes in Body Mass and Adiposity

Objective: To investigate the familial resemblance of 7‐year changes in body mass and adiposity among Canadian families. Research Methods and Procedures: The sample consisted of 655 women and 660 men from 521 families who participated in the Canada Fitness Survey in 1981 and the follow‐up Campbell's Survey in 1988. Indicators of baseline and 7‐year changes in body mass and adiposity included body mass (kilograms), body mass index (BMI; kilograms per square meter), sum of five skinfolds (SF5; millimeters), and waist circumference (WC; millimeters). The data were adjusted for the effects of age and sex, and the change scores were adjusted for baseline levels. A familial correlation model was used to determine the heritability of each phenotype using maximum likelihood techniques. Results: Significant familial resemblance was observed at baseline and for 7‐year changes in all phenotypes. At baseline, moderate heritabilities were observed [body mass: heritability coefficient (h²) = 56%; BMI, h² = 39%; SF5, h² = 41%; and WC, h² = 39%], whereas values were attenuated for each change score except for WC (Δbody mass, h² = 23%; ΔBMI, h² = 14%; ΔSF5, h² = 12%; and ΔWC, h² = 45%). Discussion: Changes in body mass and adiposity significantly aggregate within families over 7 years. However, baseline values are characterized by higher heritability levels except WC. The significant heritabilities observed for change scores suggest that lifestyle, transient environmental factors, and possibly age‐related gene effects are important determinants of changes in body mass and adiposity.     

Environmental and genetic influences on body mass and resting metabolic rates (RMR) in a natural population of weasel Mustela nivalis

Body mass (BM) and resting metabolic rates (RMR) are two inexorably linked traits strongly related to mammalian life histories. Yet, there have been no studies attempting to estimate heritable variation and covariation of BM and RMR in natural populations. We used a marker‐based approach to construct a pedigree and then the ‘animal model’ to estimate narrow sense heritability (h²) of these traits in a free‐living population of weasels Mustela nivalis—a small carnivore characterised by a wide range of BM and extremely high RMR. The most important factors affecting BM of weasels were sex and habitat type, whereas RMR was significantly affected only by seasonal variation of this trait. All environmental factors had only small effect on estimates of additive genetic variance of both BM and RMR. The amount of additive genetic variance associated with BM and estimates of heritability were high and significant in males (h² = 0.61), but low and not significant in females (h² = 0.32), probably due to small sample size for the latter sex. The results from the two‐trait model revealed significant phenotypic (r_P = 0.62) and genetic correlation (r_A = 0.89) between BM and whole body RMR. The estimate of heritability of whole body RMR (0.54) and BM corrected RMR (0.45) were lower than estimates of heritability for BM. Both phenotypic and genetic correlations between BM corrected RMR and BM had negative signals (r_P = ?0.42 and r_A = ?0.58). Our results indicate that total energy expenditures of individuals can quickly evolve through concerted changes in BM and RMR.     

Genetic effects on obesity assessed by bivariate genome scan: the Mexican-American coronary artery disease study

Objective: To identify the genetic determinants of obesity using univariate and bivariate models in a genome scan. Research Methods and Procedures: We evaluated the genetic and environmental effects and performed a genome‐wide linkage analysis of obesity‐related traits in 478 subjects from 105 Mexican‐American nuclear families ascertained through a proband with documented coronary artery disease. The available obesity traits include BMI, body surface area (BSA), waist‐to‐hip ratio (WHR), and trunk fat mass as percentage of body weight. Heritability estimates and multipoint linkage analysis were performed using a variance components procedure implemented in SOLAR software. Results: The heritability estimates were 0.62 for BMI, 0.73 for BSA, 0.40 for WHR, and 0.38 for trunk fat mass as percentage of body weight. Using a bivariate genetic model, we observed significant genetic correlations between BMI and other obesity‐related traits (all p < 0.01). Evidence for univariate linkage was observed at 252 to approximately 267 cM on chromosome 2 for three obesity‐related traits (except for WHR) and at 163 to approximately 167 cM on chromosome 5 for BMI and BSA, with the maximum logarithm of the odds ratio score of 3.12 (empirical p value, 0.002) for BSA on chromosome 2. Use of the bivariate linkage model yielded an additional peak (logarithm of the odds ratio = 3.25, empirical p value, 0.002) at 25 cM on chromosome 7 for the pair of BMI and BSA. Discussion: The evidence for linkage on chromosomes 2q36‐37 and 5q36 is supported both by univariate and bivariate analysis, and an additional linkage peak at 7p15 was identified by the bivariate model. This suggests that use of the bivariate model provides additional information to identify linkage of genes responsible for obesity‐related traits.     

The effect of trait type and strength of selection on heritability and evolvability in an island bird population

The heritability (h²) of fitness traits is often low. Although this has been attributed to directional selection having eroded genetic variation in direct proportion to the strength of selection, heritability does not necessarily reflect a trait's additive genetic variance and evolutionary potential (“evolvability”). Recent studies suggest that the low h² of fitness traits in wild populations is caused not by a paucity of additive genetic variance (V_A) but by greater environmental or nonadditive genetic variance (V_R). We examined the relationship between h² and variance‐standardized selection intensities (i or β_σ), and between evolvability (I_A:V_A divided by squared phenotypic trait mean) and mean‐standardized selection gradients (β_μ). Using 24 years of data from an island population of Savannah sparrows, we show that, across diverse traits, h² declines with the strength of selection, whereas I_A and I_R (V_R divided by squared trait mean) are independent of the strength of selection. Within trait types (morphological, reproductive, life‐history), h², I_A, and I_R are all independent of the strength of selection. This indicates that certain traits have low heritability because of increased residual variance due to the age at which they are expressed or the multiple factors influencing their expression, rather than their association with fitness.     

Inheritance of size and shape in a natural population of collared flycatchers,Ficedula albicollis

Four external skeletal and three feather dimensions were measured on adult collared flycatchers (Ficedula albicollis) and their adult offspring. By using mid-offspring-midparent regressions, all traits were found to be heritable with an arithmetic mean heritability of 0.46. Heritability estimates from full-sib analyses were about 1.5 times higher (mean 0.67), indicating that variation in traits was affected by shared nest environment among full-sibs. The overall body size as measured by principal component one (PC1) was found to be heritable (h² = 0.40). However, this multivariate measure of heritability was not significant in offspring-father comparison, while highly so in offspring-mother comparison (h² = 0.60). Low offspring-father resemblance was evident also in univariate estimates of heritability. Possible causes of this (extra-pair copulations, maternal effects, sex-linked variance) are discussed. Genetic correlations among seven traits were estimated to be low (mean 0.22), and of similar magnitude or higher than phenotypic correlations (mean 0.18). All genetic correlations were positive. Genetic and phenotypic correlations as well as covariances were fairly similar to each other (r = 0.85 and r = 0.87, respectively). Environmental correlations did not follow the pattern of genetic correlations (r = 0.11), but were more similar to phenotypic correlations (r = 0.60). Given the low genetic correlations and moderate heritabilities, the overall conclusion is that the external morphology of collared flycatchers is largely under additive genetic control and that there is a strong potential for evolutionary change in morphology even under complex multivariate selection.     

RAD‐sequencing for estimating genomic relatedness matrix‐based heritability in the wild: A case study in roe deer

Estimating the evolutionary potential of quantitative traits and reliably predicting responses to selection in wild populations are important challenges in evolutionary biology. The genomic revolution has opened up opportunities for measuring relatedness among individuals with precision, enabling pedigree‐free estimation of trait heritabilities in wild populations. However, until now, most quantitative genetic studies based on a genomic relatedness matrix (GRM) have focused on long‐term monitored populations for which traditional pedigrees were also available, and have often had access to knowledge of genome sequence and variability. Here, we investigated the potential of RAD‐sequencing for estimating heritability in a free‐ranging roe deer (Capreolous capreolus) population for which no prior genomic resources were available. We propose a step‐by‐step analytical framework to optimize the quality and quantity of the genomic data and explore the impact of the single nucleotide polymorphism (SNP) calling and filtering processes on the GRM structure and GRM‐based heritability estimates. As expected, our results show that sequence coverage strongly affects the number of recovered loci, the genotyping error rate and the amount of missing data. Ultimately, this had little effect on heritability estimates and their standard errors, provided that the GRM was built from a minimum number of loci (above 7,000). Genomic relatedness matrix‐based heritability estimates thus appear robust to a moderate level of genotyping errors in the SNP data set. We also showed that quality filters, such as the removal of low‐frequency variants, affect the relatedness structure of the GRM, generating lower h² estimates. Our work illustrates the huge potential of RAD‐sequencing for estimating GRM‐based heritability in virtually any natural population.     

Heritability of body size in the polar bears of Western Hudson Bay

Among polar bears (Ursus maritimus), fitness is dependent on body size through males’ abilities to win mates, females’ abilities to provide for their young and all bears’ abilities to survive increasingly longer fasting periods caused by climate change. In the Western Hudson Bay subpopulation (near Churchill, Manitoba, Canada), polar bears have declined in body size and condition, but nothing is known about the genetic underpinnings of body size variation, which may be subject to natural selection. Here, we combine a 4449‐individual pedigree and an array of 5,433 single nucleotide polymorphisms (SNPs) to provide the first quantitative genetic study of polar bears. We used animal models to estimate heritability (h²) among polar bears handled between 1966 and 2011, obtaining h² estimates of 0.34–0.48 for strictly skeletal traits and 0.18 for axillary girth (which is also dependent on fatness). We genotyped 859 individuals with the SNP array to test for marker–trait association and combined p‐values over genetic pathways using gene‐set analysis. Variation in all traits appeared to be polygenic, but we detected one region of moderately large effect size in body length near a putative noncoding RNA in an unannotated region of the genome. Gene‐set analysis suggested that variation in body length was associated with genes in the regulatory cascade of cyclin expression, which has previously been associated with body size in mice. A greater understanding of the genetic architecture of body size variation will be valuable in understanding the potential for adaptation in polar bear populations challenged by climate change.     

Evidence of Shared Genetic Effects Between Pre‐ and Postobesity Epidemic BMI Levels

United States has experienced a widespread obesity epidemic. However, it is unclear whether the obesogenic environment has uncovered genes previously unimportant in adiposity or whether genes influencing obesity are the same before and after the obesity epidemic. The objective of this study was to test whether BMI pre‐ and postobesity epidemic would be controlled by shared genetic effects. A 25–30‐year follow‐up of parents and children who participated in the National Institutes of Health–National Heart, Lung, and Blood Institute Lipid Research Clinics (LRC) Princeton School Study, 1973–1976, were followed up in 1999–2004 in the Princeton Follow‐up Study (PFS). Heritability of BMI and genetic correlations between pre‐epidemic BMI and BMI z‐scores in adolescents and postobesity epidemic BMI were calculated. Even though they had similar ages, offspring had higher BMI in PFS than their parents in LRC (28.5 ± 6.6 vs. 26.1 ± 4.4, P < 0.0001). BMI measurements in offspring were strongly heritable (BMI_LRC: h² = 0.78 ± 0.17; BMI z‐score_LRC: h² = 0.61 ± 0.16; BMI_PFS: h² = 0.64 ± 0.16, all P ≤ 0.0001). Further, the change of BMI exhibited a high heritability (h² = 0.51 ± 0.18, P = 0.003). Bivariate analysis of BMI in LRC and PFS showed significant genetic correlation (0.70 ± 0.16, P = 0.005), whereas the environmental correlation was not significant (0.36 ± 0.17). Although the obesogenic environment may have changed between the 1970s and 2000s, many of the same genes are likely to be involved in establishing genetic susceptibility to obesity. Furthermore, shared genetic effects survive the period of the transition from adolescence to adulthood.     

Evolutionary potential of thermal preference and heat tolerance in Drosophila subobscura

Evolutionary change of thermal traits (i.e., heat tolerance and behavioural thermoregulation) is one of the most important mechanisms exhibited by organisms to respond to global warming. However, the evolutionary potential of heat tolerance, estimated as narrow‐sense heritability, depends on the methodology employed. An alternative adaptive mechanism to buffer extreme temperatures is behavioural thermoregulation, although the association between heat tolerance and thermal preference is not clearly understood. We suspect that methodological effects associated with the duration of heat stress during thermal tolerance assays are responsible for missing this genetic association. To test this hypothesis, we estimated the heritabilities and genetic correlations for thermal traits in Drosophila subobscura, using high‐temperature static and slow ramping assays. We found that heritability for heat tolerance was higher in static assays (h² = 0.134) than in slow ramping assays (h² = 0.084), suggesting that fast assays may provide a more precise estimation of the genetic variation of heat tolerance. In addition, thermal preference exhibited a low heritability (h² = 0.066), suggesting a reduced evolutionary response for this trait. We also found that the different estimates of heat tolerance and thermal preference were not genetically correlated, regardless of how heat tolerance was estimated. In conclusion, our data suggest that these thermal traits can evolve independently in this species. In agreement with previous evidence, these results indicate that methodology may have an important impact on genetic estimates of heat tolerance and that fast assays are more likely to detect the genetic component of heat tolerance.     

Total and Regional Fat Distribution is Strongly Influenced by Genetic Factors in Young and Elderly Twins

Objective: Indirect estimates of obesity such as BMI seem to be strongly influenced by genetic factors in twins. Precise measurements of total and regional fat as determined by direct techniques such as DXA scan have only been applied in a few twin studies. The aim of the present study was to estimate the heritability (h²) of total and regional fat distribution in young and elderly Danish twins. Research Methods and Procedures: Monozygotic (108) and dizygotic (88) twins in two age groups (25 to 32 and 58 to 66 years) underwent anthropometric measurements and DXA scans. Intraclass correlations and etiologic components of variance were estimated for total and regional fat percentages using biometric modeling. Results: The intraclass correlations demonstrated higher correlations for all fat percentages among monozygotic twins as compared with dizygotic twins. The biometric modeling revealed a major genetic component (h²) of total (h²_young = 0.83, h²_elderly = 0.86) and regional fat percentages (trunk, h²_young = 0.82, h²_elderly = 0.85; lower body, h²_young = 0.83, h²_elderly = 0.81; and trunk/lower body, h²_young = 0.83, h²_elderly = 0.71) in both the young and elderly twins. Discussion: The h² estimates emphasize that body fat and distribution as determined by DXA scan are under extensive genetic control.     

Natural selection on the genetical component of variance in body condition in a wild bird population

Although there is substantial evidence that skeletal measures of body size are heritable in wild animal populations, it is frequently assumed that the nonskeletal component of body weight (or ‘condition’) is determined primarily by environmental factors, in particular nutritional state. We tested this assumption by quantifying the genetic and environmental components of variance in fledgling body condition index (=relative body weight) in a natural population of collared flycatchers (Ficedula albicollis), and compared the strength of natural selection on individual breeding values with that on phenotypic values. A mixed model analysis of the components of variance, based on an ‘animal model’ and using 18 years of data on 17 717 nestlings, revealed a significant additive genetic component of variance in body condition, which corresponded to a narrow sense heritability (h²) of 0.30 (SE=0.03). Nongenetic contributions to variation in body condition were large, but there was no evidence of dominance variance nor of contributions from early maternal or common environment effects (pre‐manipulation environment) in condition at fledging. Comparison of pre‐ and post‐selection samples revealed virtually identical h² of body condition index, despite the fact that there was a significant decrease (35%) in the levels of additive genetic variance from fledging to breeding. The similar h² in the two samples occurred because the environmental component of variance was also reduced by selection, suggesting that natural selection was acting on both genotypic and environmental variation. The effects of selection on genetic variance were confirmed by calculation of the selection differentials for both phenotypic values and best linear unbiased predictor (BLUP) estimates of breeding values: there was positive directional selection on condition index both at the phenotypic and the genotypic level. The significant h² of body condition index is consistent with data from human and rodent populations showing significant additive genetic variance in relative body mass and adiposity, but contrasts with the common assumption in ecology that body condition reflects an individual’s nongenetic nutritional state. Furthermore, the substantial reduction in the additive genetic component of variance in body condition index suggests that selection on environmental deviations cannot alone explain the maintenance of additive genetic variation in heritable traits, but that other mechanisms are needed to explain the moderate to high heritabilities of traits under consistent and strong directional selection.     

Genetic Epidemiology of BMI and Body Mass Change From Adolescence to Young Adulthood

The complex interplay between genes and environment affecting body mass gain over lifecycle periods of risk is not well understood. We use longitudinal sibling cohort data to examine the role of shared household environment, additive genetic, and shared genetic effects on BMI and BMI change. In the National Longitudinal Study of Adolescent Health, siblings and twin pairs sharing households for ≥10 years as adolescents (N = 5,524; mean = 16.5 ± 1.7 years) were followed into young adulthood (N = 4,368; mean = 22.4 ± 1.8 years). Using a variance component approach, we quantified genetic and household effects on BMI in siblings and nonsiblings sharing household environments over time. Adjusting for race, age, sex, and age‐by‐sex interaction, we detected a heritability of 0.43 ± 0.05 for BMI change. Significant household effects were noted during the young adulthood period only (0.11 ± 0.06). We find evidence for shared genetic effects between BMI and BMI change during adolescence (genetic correlation (ρ_G) = 0.61 ± 0.03) and young adulthood (ρ_G = 0.23 ± 0.06). Our findings support a complex etiology of BMI and BMI change.     

The influence of nonrandom extra‐pair paternity on heritability estimates derived from wild pedigrees

Quantitative genetic analysis is often fundamental for understanding evolutionary processes in wild populations. Avian populations provide a model system due to the relative ease of inferring relatedness among individuals through observation. However, extra‐pair paternity (EPP) creates erroneous links within the social pedigree. Previous work has suggested this causes minor underestimation of heritability if paternal misassignment is random and hence not influenced by the trait being studied. Nevertheless, much literature suggests numerous traits are associated with EPP and the accuracy of heritability estimates for such traits remains unexplored. We show analytically how nonrandom pedigree errors can influence heritability estimates. Then, combining empirical data from a large great tit (Parus major) pedigree with simulations, we assess how heritability estimates derived from social pedigrees change depending on the mode of the relationship between EPP and the focal trait. We show that the magnitude of the underestimation is typically small (<15%). Hence, our analyses suggest that quantitative genetic inference from pedigrees derived from observations of social relationships is relatively robust; our approach also provides a widely applicable method for assessing the consequences of nonrandom EPP.     

Estimation of additive genetic variance in commercial layer poultry and simulated populations under selection

Changes in genetic parameters over generations for a selected commercial population and simulated populations of poultry with different sizes were studied. The traits analyzed from the commercial population were rate of lay, age at first egg, egg weight, deformation, and body weight. In the simulated population, a trait measured on both sexes and a sex-limited trait, measured only on one sex, each with a heritability of 0.1 and 0.5, were analyzed. In the commercial and simulated populations, males and females were selected on the basis of family selection indexes and data was available only after many generations of selection. Parameters for each generation were estimated by fitting an animal model using derivative free maximum likelihood (DFREML) with different data structures. In structure 1, data included the given (base) generation for which the parameters were to be estimated, and all subsequent generations. In structure 2, only data on birds in the given generation and their progeny were included. In both structures, parents of base-generation birds were assumed unrelated and pedigrees traced back to these parents. With commercial data using structure 1, estimates of _a ² and h² decreased by 14 to 37% across five generations. With structure 2, no trends were observed, though estimates were lower than for structure 1. For simulated data, with a heritability of 0.1, both structures yielded apparently unbiased estimates of the observed additive genetic variances in the (selected) base generation, no matter how many generations of data were utilized, for both sex-limited and normal traits. However, with a heritability of 0.5 the estimated additive genetic variance for both types of trait decreased with a decrease in the number of generations used in the estimation. Estimates based on the first two generations underestimated, while estimates based on five generations of data overestimated, the observed genetic variances in the defined base. The combinations of conditions that lead to varying degrees of bias remain undefined.     

Estimation of genetic variability and heritability for biofuel feedstock yield in several populations of switchgrass

Information on heritability and predicted gains from selection for increased biomass yield for ethanol production in switchgrass is limited and may vary among breeding populations. The purpose of this study was to estimate heritability and predicted gains from selection for higher biomass yield within a lowland ecotype switchgrass population, Southern Lowland 93 (SL‐93), and two upland ecotype switchgrass populations, Southern Upland Northern Upland Early Maturing (SNU‐EM) and Southern Upland Northern Upland Late Maturing (SNU‐LM). Narrow‐sense heritabilities (h_n²) for biomass yield in each of the three populations were estimated via progeny–parent regression analysis. Half‐sib (HS) progeny families from 130 randomly selected plants from the SL‐93 population were evaluated for biomass yield in replicated trials in 2002 and 2003. Clonal parent plants were evaluated for biomass yield in separate environments to provide unbiased h_n² estimates from progeny–parent regression. Yield differences were highly significant among SL‐93 HS progenies within and over years. For the SL‐93 population, h_n² estimates were 0.13 and 0.12 based on individual plant and phenotypic family mean (PFM) selection, respectively. Predicted genetic gains (ΔG) per selection cycle were 0.15 kg dry matter (dm) plant^?1 and 0.10 kg dm plant^?1 for PFM and individual plant selection methods, respectively. For the SNU‐EM and SNU‐LM populations, year and year × HS family effects were highly significant (P < 0.01) and the HS family effect over years was nonsignificant (P < 0.05). However, HS family effects were highly significant within respective years (P < 0.01). Estimates of h_n² for the SNU‐EM and SNU‐LM populations based on PFM and individual plant selection were similar, ranging from 0.44 to 0.47; ΔG per selection cycle ranged from 0.22 to 0.33 kg dm plant^?1. The magnitudes of the estimates of additive genetic variation suggest that selection for higher biomass yield should be possible. The substantial effect of environment on biomass yields in the upland populations and the failure of families to respond similarly over years stress the importance of adequately testing biomass yield over years to assess yield.     

Heritability of Body Composition Measured by DXA in the Diabetes Heart Study

Objective: The purpose of this study was to investigate the heritability of body composition measured by DXA in the Diabetes Heart Study (DHS). Research Methods and Procedures: Participants were 292 women and 262 men (age, 38 to 86 years; BMI, 17 to 57 kg/m²) from 244 families. There were 492 white and 49 African‐American sibling pairs. DXA measurements of percentage fat mass (FM), whole body FM, and lean mass (LM), as well as regional measurements of trunk fat mass (TFM) and appendicular lean mass (ALM), were obtained. Heritability of FM, LM, and BMI were estimated using Sequential Oligogenic Linkage Analysis Routines. Results: After adjusting for age, gender, ethnicity, and height, the heritability estimates of various compositional attributes were %FM = 0.64, whole body FM = 0.71, TFM = 0.63, whole body LM = 0.60, ALM = 0.66, and BMI = 0.64 (all p < 0.0001). Additional adjustment for diabetes status, smoking, dietary intake, and physical activity resulted in only minor changes in the heritability estimates (?² = 0.63 to 0.72, all p < 0.0001). Furthermore, heritability of TFM after additional adjustment for whole body FM was significant (?² = 0.55, p < 0.0001), and heritability of ALM after additional adjustment for whole body LM was also significant (?² = 0.51, p < 0.0001). Discussion: These data suggest that FM and LM measured by DXA are highly heritable and can be effectively used in designing linkage studies to locate genes governing body composition. In addition, regional distribution of FM and LM may be genetically determined.     

EXPRESSION OF GENETIC VARIATION IN BODY SIZE OF THE COLLARED FLYCATCHER UNDER DIFFERENT ENVIRONMENTAL CONDITIONS

Heritability of body size in two experimentally created environments, representing good and poor feeding conditions, respectively, was estimated using cross-fostered collared flycatcher Ficedula albicollis nestlings. Young raised under poor feeding conditions attained smaller body size (tarsus length) than their full-sibs raised under good feeding conditions. Parent-offspring regressions revealed lower heritability (h²) of body size under poor than under good feeding conditions. Hence, as the same set of parents were used in the estimation of h² in both environments, this suggests environment-dependent change in additive genetic component of variance (V_A), or that the genetic correlation between parental and poor offspring environment was less than that between parental and good offspring environment. However, full-sib analyses failed to find evidence for genotype-environment interactions, although the power of these tests might have been low. Full-sib heritabilities in both environments tended to be higher than estimates from parent-offspring regressions, indicating that prehatching or early posthatching common environment/maternal effects might have inflated full-sib estimates of V_A. The effect of sibling competition on estimates of V_A was probably small as the nestling size-hierarchy at day 2 posthatch was not generally correlated with size-hierarchy at fledging. Furthermore, there was no correlation between maternal body condition during the incubation and final size of offspring, indicating that direct maternal effects related to nutritional status were small. A review of earlier quantitative genetic studies of body size variation in birds revealed that in eight of nine cases, heritability of body size was lower in poor than in good environmental conditions. The main implication of this relationship will be a decreased evolutionary response to selection under poor environmental conditions. On the other hand, this will retard the loss of genetic variation by reducing the accuracy of selection and might help explain the moderate to high heritabilities of body-size traits under good environmental conditions.     

Genome-wide scan of plasma cholecystokinin in baboons shows linkage to human chromosome 17

Objective: Cholecystokinin (CCK) is known to inhibit food intake and is an important signal for controlling meal volume, indicating a possible role in weight regulation. Our objective was to investigate genetic influences on plasma CCK in baboons. Research Methods and Procedures: Subjects were 376 baboons (males = 113, females = 263) from the Southwest National Primate Research Center, housed at the Southwest Foundation for Biomedical Research, San Antonio, Texas. Anthropometric and biochemical parameters were analyzed. Genetic effects on plasma CCK were estimated by the maximum likelihood‐based variance components method implemented in the software program SOLAR (Sequential Oligogenic Linkage Analysis Routines). Results: Male baboons (32.7 ± 6 kg) were much heavier than females (20.2 ± 4 kg). Similarly, mean (± standard deviation) plasma CCK values were also higher in male baboons (13.8 ± 6 pM) than female baboons (12.5 ± 4 pM). Significant heritabilities were observed for plasma CCK (0.14 ± 0.1, p < 0.05), body weight (h² = 0.62 ± 0.15, p < 10^?8), and glucose (h² = 0.68 ± 0.17, p < 10^?7). A genome‐wide scan of plasma CCK detected a strong signal for a quantitative trait locus (QTL) on chromosome 17p12–13 [logarithm of the odds (LOD) = 3.1] near marker D17S804. Suggestive evidence of a second QTL was observed on chromosome 4q34–35 (LOD = 2.3) near marker D4S2374. Discussion: A substantial contribution of additive genetic effects to the variation in plasma levels of CCK was demonstrated in baboons. The identification of a QTL for plasma CCK on chromosome 17p is significant, as several obesity‐related traits such as BMI, leptin, adiponectin, and acylation stimulating protein have already been mapped to this region.     

Heritability of sperm length in the bumblebee Bombus terrestris

Sperm length is highly variable, both between and within species, but the evolutionary significance of this variation is poorly understood. Sexual selection on sperm length requires a significant additive genetic variance, but few studies have actually measured this. Here we present the first estimates of narrow sense heritability of sperm length in a social insect, the bumblebee Bombus terrestris. In spite of a balanced and straightforward rearing design of colonies, and the possibility to replicate measurements of sperm within single males nested within colonies, the analysis proved to be complex. Several appropriate statistical models were derived, each depending on different assumptions. The heritability estimates obtained ranged from h ² = 0.197 ± 0.091 to h ² = 0.429 ± 0.154. All our estimates were substantially lower than previous estimates of sperm length heritability in non-social insects and vertebrates.