Showing papers in "Behavior Genetics in 2008"
TL;DR: Findings from two independent samples suggest that the association of 5-HTTLPR with depression varies according to gender and stressful life events.
Abstract: The short (s) variant of the serotonin transporter (5-HTT) gene linked functional polymorphic region (5-HTTLPR) is associated with depression. Stressful life events, gender, and race have been shown to moderate this association. We examined the relationship between 5-HTTLPR genotype and symptoms of depression in two samples. Study 1 = 288 participants from a study of caregiver stress; and Study 2 = 142 participants from a study examining psychosocial stressors, genetics, and health. Main effects of 5-HTTLPR on symptoms of depression were examined, along with moderation by stress (caregiving status or low childhood socioeconomic status (SES), gender, and race. The 5-HTTLPR × stress group × gender interaction was significant in both samples (P < 0.003, and P < 0.008, respectively). For females, the s allele, combined with caregiving stress (Study 1) or low childhood SES (Study 2), was associated with higher depression scores as compared to participants in the non-stressor group and those with the long (l) allele; whereas, in males, the l allele, combined with a stressor, was associated with higher depression scores as compared to those in the non-stressor group and those with the s allele. Findings from two independent samples suggest that the association of 5-HTTLPR with depression varies according to gender and stressful life events.
201 citations
TL;DR: The interplay between genetic liability and peer influences on the development of adolescent alcohol and tobacco use was examined using a nationally-representative sample of adolescent sibling pairs and their best friends.
Abstract: Peer relationships are commonly thought to be critical for adolescent socialization, including the development of negative health behaviors such as alcohol and tobacco use. The interplay between genetic liability and peer influences on the development of adolescent alcohol and tobacco use was examined using a nationally-representative sample of adolescent sibling pairs and their best friends. Genetic factors, some of them related to an adolescent’s own substance use and some of them independent of use, were associated with increased exposure to best friends with heavy substance use—a gene-environment correlation. Moreover, adolescents who were genetically liable to substance use were more vulnerable to the adverse influences of their best friends—a gene-environment interaction.
174 citations
TL;DR: The finding that deficits in motor timing run in ADHD-families suggests this to be a fruitful domain for further exploration in relation to the genetic underpinnings of ADHD.
Abstract: Attention-Deficit/Hyperactivity Disorder (ADHD) shares a genetic basis with motor coordination problems and probably motor timing problems. In line with this, comparable problems in motor timing should be observed in first degree relatives and might, therefore, form a suitable endophenotypic candidate. This hypothesis was investigated in 238 ADHD-families (545 children) and 147 control-families (271 children). A motor timing task was administered, in which children had to produce a 1,000 ms interval. In addition to this task, two basic motor tasks were administered to examine speed and variability of motor output, when no timing component was required. Results indicated that variability in motor timing is a useful endophenotypic candidate: It was clearly associated with ADHD, it was also present in non-affected siblings, and it correlated within families. Accuracy (under- versus over-production) in motor timing appeared less useful: Even though accuracy was associated with ADHD (probands and affected siblings had a tendency to under-produce the 1,000 ms interval compared to controls), non-affected siblings did not differ from controls and sibling correlations were only marginally significant. Slow and variable motor output without timing component also appears present in ADHD, but not in non-affected siblings, suggesting these deficits not to be related to a familial vulnerability for ADHD. Deficits in motor timing could not be explained by deficits already present in basic motor output without a timing component. This suggests abnormalities in motor timing were predominantly related to deficient motor timing processes and not to general deficient motor functioning. The finding that deficits in motor timing run in ADHD-families suggests this to be a fruitful domain for further exploration in relation to the genetic underpinnings of ADHD.
112 citations
TL;DR: This paper uses data from the National Longitudinal Study of Adolescent Health to examine the extent to which school-level social and institutional factors moderate genetic tendencies to smoke cigarettes and develops a multilevel modeling extension of regression-based quantitative genetic techniques to calculate school-specific heritability estimates.
Abstract: This paper uses data from the National Longitudinal Study of Adolescent Health to examine the extent to which school-level social and institutional factors moderate genetic tendencies to smoke cigarettes. Our analysis relies on a sub-sample of 1,198 sibling and twin pairs nested within 84 schools. We develop a multilevel modeling extension of regression-based quantitative genetic techniques to calculate school-specific heritability estimates. We show that smoking onset (h2 = .51) and daily smoking (h2 = .58) are both genetically influenced. Whereas the genetic influence on smoking onset is consistent across schools, we show that schools moderate the heritability of daily smoking. The heritability of daily smoking is the highest within schools in which the most popular students are also smokers and reduced within schools in which the majority of the students are non-Hispanic and white. These findings make important contributions to the literature on gene-environment interactions.
84 citations
TL;DR: A linear model for family resemblance is presented allowing for both genetic and cultural transmission of attitudes from parents to offspring, as well as phenotypic assortative mating and other environmental sources of twin and sibling resemblance that do not depend on the attitudes of their parents.
Abstract: The biological and social transmission of attitudes toward abortion and gay rights are analyzed in a large sample of adult twins, siblings, and their parents. We present a linear model for family resemblance allowing for both genetic and cultural transmission of attitudes from parents to offspring, as well as phenotypic assortative mating (the tendency to marry like) and other environmental sources of twin and sibling resemblance that do not depend on the attitudes of their parents. The model gives a close fit to the patterns of similarity between relatives for the two items. Results are consistent with a substantial role of genetic liability in the transmission of both attitudes. Contrary to the dominant paradigm of the social and political sciences, the kinship data are consistent with a relatively minor non-genetic impact of parental attitudes on the development of adult attitudes in their children. By contrast, the choice of mate is a social action that has a marked impact on the polarization of social attitudes and on the long-term influence that parents exert upon the next generation.
82 citations
TL;DR: It can be concluded that both genomic and nongenomic factors can tune calling behavior in mouse pups, and particularly changes in call amplitude might be of high functional relevance, since a sub-strain dependent preference towards pups emitting calls with high amplitudes was observed.
Abstract: Infant rodents emit ultrasonic vocalizations when isolated from dam and littermates. Due to the context of their occurrence and the well described bidirectional modulation by substances known for their capability to influence emotionality, it was postulated that such calls reflect a negative affective state akin anxiety. Comparative studies observed pronounced differences in calling behavior between strains, which were paralleled by differences in maternal care. Therefore, it was recently hypothesized that early environmental factors may have strong impact on call production. Here, the relative contributions of genetic background, gender, and early environmental factors on calling behavior in C57BL/6JOlaHsd and C57BL/6NCrl were studied by using an embryo-transfer procedure. The results show that these sub-strains differ in the amount of calling and specific call features, like call frequency and amplitude. The embryo-transfer procedure indicated that the observed differences in the amount of ultrasonic calling are dependent on the dyadic interaction between mother and pup. Conversely, call features were primarily dependent on the genotype of the pup. Thus, call frequency and frequency modulation were solely dependent on the pup, i.e. its genotype and gender. However, there was one exception, namely call amplitude, which was solely dependent on the genotype of the mother, i.e. on early environmental factors. Furthermore, it was shown that particularly changes in call amplitude might be of high functional relevance, since a sub-strain dependent preference towards pups emitting calls with high amplitudes was observed. In total, it can be concluded that both genomic and nongenomic factors can tune calling behavior in mouse pups.
80 citations
TL;DR: This work examines a number of closely related alternative models that do not involve gene–environment interaction but which may fit the data as well as Purcell's model and proposes one based on the correlated factors model.
Abstract: Purcell (Twin Res 5:554-571, 2002) proposed a bivariate biometric model for testing and quantifying the interaction between latent genetic influences and measured environments in the presence of gene-environment correlation. Purcell's model extends the Cholesky model to include gene-environment interaction. We examine a number of closely related alternative models that do not involve gene-environment interaction but which may fit the data as well as Purcell's model. Because failure to consider these alternatives could lead to spurious detection of gene-environment interaction, we propose alternative models for testing gene-environment interaction in the presence of gene-environment correlation, including one based on the correlated factors model. In addition, we note mathematical errors in the calculation of effect size via variance components in Purcell's model. We propose a statistical method for deriving and interpreting variance decompositions that are true to the fitted model.
79 citations
TL;DR: Analysis of the pantophysin locus (Pan I) of the same individuals revealed that individuals carrying the Pan IAA genotype are likely to display a shallow water feeding migrations while individuals carryingThe Pan IBB genotype preferred deeper waters and forage near thermal fronts, and the heterozygote exhibited both type of behaviours.
Abstract: Throughout their geographic distribution, marine fish species often form subpopulations with limited connectivity, among which individuals display a variety of migratory behaviours Fish behaviour experiments using Data Storage Tags (DSTs) have been useful to define the natural movement of individuals In Icelandic waters, such experiments have indicated the presence of two distinct behaviour types of the Atlantic cod Gadus morhua, related to vertical migrations and habitat choice in feeding migrations Some individuals have been shown to stay most of the time in shallow waters characterised by the seasonal trend in temperature for the shelf waters, while other migrate to deeper and colder waters where most of them forage in temperature fronts characterized by highly variable temperatures The analysis of the pantophysin locus (Pan I) of the same individuals revealed that individuals carrying the Pan IAA genotype are likely to display a shallow water feeding migrations while individuals carrying the Pan IBB genotype preferred deeper waters and forage near thermal fronts The heterozygote exhibited both type of behaviours This study therefore suggests that further research need to be done on the pantophysin locus and its potential effects on cod phenotypes to assess the potential relationship between this locus and the behavioural types described
78 citations
TL;DR: It is concluded that selection on breeding values for reduced LS (especially central LS) is expected to reduce reciprocal aggression and the delivery of NRA but will not change the receipt of NRA directly.
Abstract: There is increasing interest in genetic selection against behavioural traits that impact negatively on welfare and productivity in commercial livestock production. Post-mixing aggressiveness in pigs shows wide phenotypic variation, affects health, welfare and growth performance and is a routine feature of production. A Bayesian approach was used to estimate the heritability of three traits associated with aggressiveness in pigs during the 24 h post-mixing; duration in reciprocal aggression, and in receipt of, or delivery of non-reciprocal aggression (NRA). For the purposes of genetic selection, recording aggressive behaviour is excessively labour intensive. The genetic correlations were quantified between the behavioural traits and an easily measurable indicator trait; the number of skin lesions following mixing (lesion score, LS). The heritabilities for the three behavioural traits ranged from 0.17 to 0.46 (receipt of NRA and reciprocal aggression respectively). The duration in reciprocal aggression and in delivery of NRA showed a strong genetic correlation (r g = 0.79 with 95% Bayesian credibility interval of 0.62-0.94). The genetic correlation between LS and these two behaviours indicated that selection on breeding values of LS could be used to reduce aggressiveness. The duration in receipt of NRA appeared to be regulated by different genes or genomic effects compared with the other behavioural traits and LS. Although duration in receipt of NRA was not genetically associated with LS, it was lowly but significantly environmentally associated with the residuals of central and caudal LS (r e = 0.28-0.32), indicating that pigs that received NRA also received bites on the central and caudal third of the body. The pen that the animals were mixed into was found to be a very important factor for the analysed traits, in particular those representing behavioural characteristics. Based on the estimated genetic parameters, it is concluded that selection on breeding values for reduced LS (especially central LS) is expected to reduce reciprocal aggression and the delivery of NRA but will not change the receipt of NRA directly.
71 citations
TL;DR: Investigation of environmental factors that protect against or exacerbate obsessive-compulsive (OC) symptoms from a large longitudinal Dutch sample of adult twin pairs and their family members confirmed previous reports of an association of early-onset OC symptoms with higher genetic load.
Abstract: To investigate environmental factors that protect against or exacerbate obsessive-compulsive (OC) symptoms, we selected 25 monozygotic (MZ) twin pairs discordant, 17 MZ twin pairs concordant high and 34 MZ pairs concordant low on OC symptoms from a large longitudinal Dutch sample of adult twin pairs and their family members, applying stringent criteria for OC symptomatology. Data were collected on psychopathology, family structure, health, lifestyle, birth complications and life events. Unique environmental factors were studied using within-discordant MZ pair comparisons, whereas between-concordant MZ pair comparisons were used to study environmental factors that are shared by the twins of an MZ pair. The high-scoring MZ twins of the discordant group reported more life events (especially sexual abuse) than their low-scoring twin-siblings. The between-pair comparisons showed lower birth weight in the discordant MZ pairs than in the concordant MZ pairs. Further, the concordant high MZ pairs as well as their spouses had a lower educational level than the two other groups. On scale scores of anxious-depression, neuroticism, and somatic complaints, concordant high MZ pairs showed highest scores, and the discordant MZ pairs scored intermediate, except for neuroticism, on which the high-scoring twins of discordant MZ pairs were equal to the concordant high pairs. Discordance on psychological scale scores between the concordant MZ pairs was evident from 1991 onward, and within the discordant MZ pairs from 1997 onward, confirming previous reports of an association of early-onset OC symptoms with higher genetic load. Parent scores of OC symptoms and anxious-depression suggested intermediate genetic load in the discordant MZ group. In conclusion, this study reports on both unique and shared environmental factors associated with OC symptomatology. Whether these factors operate in addition to or in interaction with genetic disposition is to be elucidated in future studies.
70 citations
TL;DR: The genetic overlap between questionnaire ratings and the DSM-IV diagnosis of ADHD is high and the genetic correlations among the measures collected at age 12 varied between .63 and 1.00.
Abstract: Objective The assessment of symptoms of ADHD in children is usually based on a clinical interview or a behavior checklist. The aim of the present study is to investigate the extent to which these instruments measure an underlying construct and to estimate the genetic and environmental influences on individual differences in ADHD. Methods Maternal ratings were collected on 10,916 twins from 5,458 families. Child Behavior Checklist (CBCL) ratings were available for 10,018, 6,565, and 5,780 twins at the ages 7, 10, and 12, respectively. The Conners Rating Scale (4,887 twins) and the DSM interview (1,006 twins) were completed at age 12. The magnitude of genetic and environmental influences on the variance of the three measures of ADHD and the covariance among the three measures of ADHD was obtained. Results Phenotypic correlations range between .45 and .77. Variances and covariances of the measurements were explained mainly by genetic influences. The model that provided the best account of the data included an independent pathway for additive and dominant genetic effects. The genetic correlations among the measures collected at age 12 varied between .63 and 1.00. Conclusions The genetic overlap between questionnaire ratings and the DSM-IV diagnosis of ADHD is high. Clinical and research implications of these findings are presented.
TL;DR: Direct observations and differences in long-term insemination rates show that the loss of the sex comb strongly reduces the ability of males to copulate with females, and detailed analysis of video recordings indicates this effect is not due to changes in the males’ courtship behavior.
Abstract: The sex comb is one of the most rapidly evolving male-specific traits in Drosophila, making it an attractive model to study sexual selection and developmental evolution. Drosophila males use their sex combs to grasp the females' abdomen and genitalia and to spread their wings prior to copulation. To test the role of this structure in male mating success in Drosophila melanogaster, we genetically ablated the sex comb by expressing the female-specific isoform of the sex determination gene transformer in the tarsal segments of male legs. This technique does not remove the sex comb entirely, but simply restores the morphology of its constituent bristles to the ancestral condition found in Drosophila species that lack sex combs. Direct observations and differences in long-term insemination rates show that the loss of the sex comb strongly reduces the ability of males to copulate with females. Detailed analysis of video recordings indicates that this effect is not due to changes in the males' courtship behavior. Rapid evolution of sex comb morphology may be driven either by changes in female preferences, or by co-evolution between sex combs and female external genitalia.
TL;DR: It is suggested that premutation carriers may be at risk for emotional morbidity; however, phenotypic differences were subtle and of small effect size.
Abstract: The fragile X disorder spectrum, due to a CGG expansion in FMR1, includes fragile X syndrome (>200 repeats) and the premutation-associated disorders of ovarian insufficiency and tremor/ataxia syndrome (~55–199 repeats). Altered neurobehavioral profiles including variation of phenotypes associated with mood and anxiety may be expected among younger premutation carriers given this spectrum of disorders. However, previous studies have produced conflicting findings, providing the motivation to examine these phenotypes further. We investigated measures of mood and anxiety in 119 males and 446 females age 18–50 ascertained from families with a history of fragile X syndrome and from the general population. Scores were analyzed using a linear model with repeat length as the main predictor, adjusting for potential confounders. Repeat length was not associated with anxiety, but was marginally associated with depression and negative affect in males and negative affect only in females. These results suggest that premutation carriers may be at risk for emotional morbidity; however, phenotypic differences were subtle and of small effect size.
TL;DR: Gene-environment interaction was studied in a sample of young and older adult males and females and showed increased common environmental variation in older males whose parents were more highly educated, and increased unique environmental effects in Older males living in more affluent areas.
Abstract: Gene-environment interaction was studied in a sample of young (mean age 26 years, N = 385) and older (mean age 49 years, N = 370) adult males and females. Full scale IQ scores (FSIQ) were analyzed using biometric models in which additive genetic (A), common environmental (C), and unique environmental (E) effects were allowed to depend on environmental measures. Moderators under study were parental and partner educational level, as well as urbanization level and mean real estate price of the participants’ residential area. Mean effects were observed for parental education, partner education and urbanization level. On average, FSIQ scores were roughly 5 points higher in participants with highly educated parents, compared to participants whose parents were less well educated. In older participants, IQ scores were about 2 points higher when their partners were highly educated. In younger males, higher urbanization levels were associated with slightly higher FSIQ scores. Our analyses also showed increased common environmental variation in older males whose parents were more highly educated, and increased unique environmental effects in older males living in more affluent areas. Contrary to studies in children, however, the variance attributable to additive genetic effects was stable across all levels of the moderators under study. Most results were replicated for VIQ and PIQ.
TL;DR: A method to measure fox behavior as quantitative phenotypes which distinguish populations and resegregate in experimental pedigrees is described, which should provide new insights into the mechanisms of mammalian behavior and canine domestication.
Abstract: Strains of silver foxes, selectively bred at the Institute of Cytology and Genetics of the Russian Academy of Sciences, are a well established, novel model for studying the genetic basis of behavior, and the processes involved in canine domestication. Here we describe a method to measure fox behavior as quantitative phenotypes which distinguish populations and resegregate in experimental pedigrees. We defined 50 binary observations that nonredundantly and accurately distinguished behaviors in reference populations and cross-bred pedigrees. Principal-component analysis dissected out the independent elements underlying these behaviors. PC1 accounted for >44% of the total variance in measured traits. This system clearly distinguished tame foxes from aggressive and wildtype foxes. F1 foxes yield intermediate values that extend into the ranges of both the tame and aggressive foxes, while the scores of the backcross generation resegregate. These measures can thus be used for QTL mapping to explore the genetic basis of tame and aggressive behavior in foxes, which should provide new insights into the mechanisms of mammalian behavior and canine domestication.
TL;DR: The tryptophan hydroxylase 2 gene (TPH2) was resequenced at the 5′ upstream, coding, and 3′ downstream regions, including all 11 exons in 185 subjects, and a significant association with vulnerability to develop heroin addiction was found.
Abstract: The tryptophan hydroxylase 2 gene (TPH2) was resequenced at the 5′ upstream, coding, and 3′ downstream regions, including all 11 exons in 185 subjects. Twenty-three novel and 14 known variants were identified. In a cohort of 583 consecutively ascertained subjects, including normal volunteers and those with specific addictive diseases, six common TPH2 and one TPH1 variant were genotyped. Allele frequencies of three TPH2 variants and the TPH1 variant varied significantly among the four ethnic groups within the control subjects. Of these subjects, 385 who met heroin addiction or control criteria and were of Caucasian, African-American, or Hispanic ethnicity were examined for potential association with vulnerability to develop heroin addiction. At the two locus genotype level in Hispanics, the TPH1 rs1799913 variant was found to significantly interact with the TPH2 rs7963720 variant and heroin addiction (P = 0.022), and with the TPH2 rs4290270 variant and heroin addiction (P = 0.011). In the African-American group, a significant association of a specific TPH2 haplotype with heroin addiction also was found (SNPHAP, P = 0.004; PHASE P = 0.036).
TL;DR: Phenotypic correlations across measures were modest, but a common underlying phenotypic factor was highly heritable, as was a simple aggregation of all three measurements, which suggests that distilling what is common to all three measures may be a good method for generating a quantitative trait suitable for molecular studies of activity level in children.
Abstract: Despite the high heritability of children's activity level, which forms part of the core symptom domain of hyperactivity-impulsivity within attention deficit hyperactivity disorder (ADHD), there has only been a limited success with identifying candidate genes involved in its etiology. This may reflect a lack of understanding about the different measures used to define activity level across studies. We aimed to study the genetic and environmental etiology across three measures of activity level: parent and teacher ratings of hyperactivity-impulsivity and actigraph measurements, within a population-based sample of 463 7-9 year old twin pairs. We further examined ways in which the three measures could be combined for future molecular studies. Phenotypic correlations across measures were modest, but a common underlying phenotypic factor was highly heritable (92%); as was a simple aggregation of all three measurements (77%). This suggests that distilling what is common to all three measures may be a good method for generating a quantitative trait suitable for molecular studies of activity level in children. The high heritabilities found are encouraging in this respect.
TL;DR: The stability of WB was largely explained by genetic effects, accounting for 74% of stability in boys and 65% in girls, and most shared environmental effects were common to both raters, suggesting little influence of rater bias in the assessment of WB.
Abstract: We examined the contribution of genetic and environmental influences on the stability of withdrawn behavior (WB) in childhood using a longitudinal multiple rater twin design. Maternal and paternal ratings on the withdrawn subscale of the Child Behavior Checklist (CBCL) were obtained from 14,889 families when the twins were 3, 7, 10 and 12 years old. A longitudinal psychometric model was fitted to the data and the fit of transmission and common factor models were evaluated for each variance component. WB showed considerable stability throughout childhood, with correlation coefficients ranging from about .30 for the 9-year time interval to .65 for shorter time intervals. Individual differences in WB as observed by the mother and the father were found to be largely influenced by genetic effects at all four time points, in both boys (50–66%) and girls (38–64%). Shared environmental influences explained a small to modest proportion (0–24%) of the variance at all ages and were slightly more pronounced in girls. Non-shared environmental influences were of moderate importance to the variance and slightly increased with age, from 22–28% at age 3 to 35–41% at age 12 years. The stability of WB was largely explained by genetic effects, accounting for 74% of stability in boys and 65% in girls. Shared environmental effects explained 7% (boys) and 17% (girls) of the behavioral stability. Most shared environmental effects were common to both raters, suggesting little influence of rater bias in the assessment of WB. The shared environmental effects common to both raters were best described by a common factor model, indicating that these effects are stable and persistent throughout childhood. Non-shared environmental effects accounted for the remaining covariance over time.
TL;DR: The aim of this study was to model birth weights of twins across gestational age and to quantify the genetic and environmental components to reduce the common environmental variance to increase heritability and thereby the chance of identifying candidate genes influencing the genetic variance of birth weight.
Abstract: Heritability estimates of birth weight have been inconsistent Possible explanations are heritability changes during gestational age or the influence of covariates (eg chorionicity) The aim of this study was to model birth weights of twins across gestational age and to quantify the genetic and environmental components We intended to reduce the common environmental variance to increase heritability and thereby the chance of identifying candidate genes influencing the genetic variance of birth weight Perinatal data were obtained from 4232 live-born twin pairs from the East Flanders Prospective Twin Survey, Belgium Heritability of birth weights across gestational ages was estimated using a non-linear multivariate Gaussian regression with covariates in the means model and in covariance structure Maternal, twin-specific, and placental factors were considered as covariates Heritability of birth weight decreased during gestation from 25 to 42 weeks However, adjusting for covariates increased the heritability over this time period, with the highest heritability for first-born twins of multipara with separate placentas, who were staying alive (from 52% at 25 weeks to 30% at 42 weeks) Twin-specific factors revealed latent genetic components, whereas placental factors explained common and unique environmental factors The number of placentas and site of the insertion of the umbilical cord masked the effect of chorionicity Modeling genetic and environmental factors leads to a better estimate of their role in growth during gestation For birth weight, mainly environmental factors were explained, resulting in an increase of the heritability and thereby the chance of finding genes influencing birth weight in linkage and association studies
TL;DR: The genotype × gender interaction was a significant predictor of depression-dejection, and trended towards predicting anger−hostility during TRP infusion, and males in the HiHi group had greater increases in negative affect during infusion, compared to all groups except LoLo females, who also showed increased negative affect.
Abstract: Expression of the serotonin transporter is affected by the genotype of the 5-HTTLPR (short and long forms) as well as the genotype of the SNP rs25531 within this region. Based on the combined genotypes for these polymorphisms, we designated each allele as a high or low expressing allele according to established expression levels—resulting in HiHi, HiLo, & LoLo genotype groups for analysis. We evaluated effects of gender and the promoter genotype on induction of negative affect by intravenous infusion of l-tryptophan (TRP). The protocol consisted of a day-1 sham saline infusion and a day-2 active TRP infusion. Models assessed 5-HTTLPR composite genotype and gender as predictors of change in ratings of negative emotion during TRP infusion. During sham infusion there were no significant changes from baseline in mood ratings. During TRP infusion all negative affect ratings increased significantly from baseline (P’s < .02). The genotype × gender interaction was a significant predictor of depression-dejection (P = .013), and trended towards predicting anger−hostility (P = .084). Males in the HiHi group had greater increases in negative affect during infusion, compared to all groups except LoLo females, who also showed increased negative affect.
TL;DR: It is suggested that genetic characteristics can impact the way an individual experiences its social environment and that female macaques that are homozygous at two microsatellite loci appear to be less attractive social partners based on grooming and aggression received by unrelated conspecifics.
Abstract: The relationship between an individual’s genotype and its phenotype is a central issue in biology, but one that is largely unexplored for the important phenotype of complex social behavior. Here we examine the relationship between heterozygosity and social behavior among unrelated adult female rhesus macaques living on the island of Cayo Santiago (Puerto Rico). We show that female macaques with lower mean neutral heterozygosity were discriminated against by their unrelated conspecifics: less heterozygous females received aggressive behavior at higher rates and received affiliation at lower rates than more heterozygous females. We demonstrate that these results are likely due to local genomic effects associated with particular microsatellite loci. Our study suggests that genetic characteristics can impact the way an individual experiences its social environment and that female macaques that are homozygous at two microsatellite loci appear to be less attractive social partners based on grooming and aggression received by unrelated conspecifics.
TL;DR: Examination of additive and non-additive genetic contributions to the personality trait of extraversion in 1,689 Dutch twin pairs, 1,505 mothers and 1,637 fathers of the twins shows that in addition to additive genetic influences,extraversion in adolescents is influenced by non- additive genetic factors.
Abstract: The influence of non-additive genetic influences on personality traits has been increasingly reported in adult populations. Less is known, however, with respect to younger samples. In this study, we examine additive and non-additive genetic contributions to the personality trait of extraversion in 1,689 Dutch twin pairs, 1,505 mothers and 1,637 fathers of the twins. The twins were on average 15.5 years (range 12–18 years). To increase statistical power to detect non-additive genetic influences, data on extraversion were also collected in parents and simultaneously analyzed. Genetic modeling procedures incorporating age as a potential modifier of heritability showed significant influences of additive (20–23%) and non-additive genetic factors (31–33%) in addition to unshared environment (46–48%) for adolescents and for their parents. The additive genetic component was slightly and positively related to age. No significant sex differences were found for either extraversion means or for the magnitude of the genetic and environmental influences. There was no evidence of non-random mating for extraversion in the parental generation. Results show that in addition to additive genetic influences, extraversion in adolescents is influenced by non-additive genetic factors.
TL;DR: The results suggest that variation in attitudes toward homosexuality is substantially inherited, and that social environmental influences are relatively minor.
Abstract: Previous research has shown that many heterosexuals hold negative attitudes toward homosexuals and homosexuality (homophobia). Although a great deal of research has focused on the profile of homophobic individuals, this research provides little theoretical insight into the aetiology of homophobia. To examine genetic and environmental influences on variation in attitudes toward homophobia, we analysed data from 4,688 twins who completed a questionnaire concerning sexual behaviour and attitudes, including attitudes toward homosexuality. Results show that, in accordance with literature, males have significantly more negative attitudes toward homosexuality than females and non-heterosexuals are less homophobic than heterosexuals. In contrast with some earlier findings, age had no significant effect on the homophobia scores in this study. Genetic modelling showed that variation in homophobia scores could be explained by additive genetic (36%), shared environmental (18%) and unique environmental factors (46%). However, corrections based on previous findings show that the shared environmental estimate may be almost entirely accounted for as extra additive genetic variance arising from assortative mating for homophobic attitudes. The results suggest that variation in attitudes toward homosexuality is substantially inherited, and that social environmental influences are relatively minor.
TL;DR: Estimating the relative contributions of genetic and environmental effects to variation in the perceived intensity and pleasantness of cinnamon, chocolate, turpentine, and isovaleric acid (sweaty) odors by quantitative genetic modeling of odor rating data from 856 twin individuals promotes the importance of inter-individual variation in odor exposures and olfactory plasticity to odor perception.
Abstract: Human genes encoding odorant receptors have been identified, but the contribution of genetic effects to total variation in specific odor perceptions is largely unknown. We estimated the relative contributions of genetic and environmental effects to variation in the perceived intensity and pleasantness of cinnamon, chocolate, turpentine, and isovaleric acid (sweaty) odors by quantitative genetic modeling of odor rating data from 856 twin individuals (including 83 complete monozygotic and 275 dizygotic twin pairs) aged 10-60 years (44% males and 56% females) from Australia, Denmark, and Finland. Results from fitting univariate models including components for additive genetic (A), shared environmental (C), and non-shared environmental (E) effects to the data implied that non-shared environmental effects account for the most variation in ratings of individual odors while genetic effects play only a minor role. Multivariate independent pathway model revealed a modest but significant common additive genetic component for intensity ratings, explaining 18% of the total variation. The results promote the importance of inter-individual variation in odor exposures and olfactory plasticity to odor perception.
TL;DR: It is unlikely that four genes of the canine serotonergic system, coding for the serotonin receptors 1A, 1B, and 2A, and the serotonin transporter, could play a major role in aggression in Golden Retriever dogs.
Abstract: Aggressive behavior displays a high heritability in our study group of Golden Retriever dogs. Alterations in brain serotonin metabolism have been described in aggressive dogs before. Here, we evaluate whether four genes of the canine serotonergic system, coding for the serotonin receptors 1A, 1B, and 2A, and the serotonin transporter, could play a major role in aggression in Golden Retrievers. We performed mutation screens, linkage analysis, an association study, and a quantitative genetic analysis. There was no systematic difference between the coding DNA sequence of the candidate genes in aggressive and non-aggressive Golden Retrievers. An affecteds-only parametric linkage analysis revealed no strong major locus effect on human-directed aggression related to the candidate genes. An analysis of 41 single nucleotide polymorphisms (SNPs) in the 1 Mb regions flanking the genes in 49 unrelated human-directed aggressive and 49 unrelated non-aggressive dogs did not show association of SNP alleles, genotypes, or haplotypes with aggression at the candidate loci. We completed our analyses with a study of the effect of variation in the candidate genes on a collection of aggression-related phenotypic measures. The effects of the candidate gene haplotypes were estimated using the Restricted Maximum Likelihood method, with the haplotypes included as fixed effects in a linear animal model. We observed no effect of the candidate gene haplotypes on a range of aggression-related phenotypes, thus extending our conclusions to several types of aggressive behavior. We conclude that it is unlikely that these genes play a major role in the variation in aggression in the Golden Retrievers that we studied. Smaller phenotypic effects of these loci could not be ruled out with our sample size.
TL;DR: The mHB test gave evidence that Slc2a8−/− mice exhibit a reduced risk assessment because they performed less rearings in an unprotected area and showed significantly reduced latency to stretched body posture, suggesting that behavioral alterations of Slc 2a8+/- mice are due to dysfunctions in neuronal processes presumably as a consequence of defects in the glucose metabolism.
Abstract: Transport of glucose into neuronal cells is predominantly mediated by the glucose transporters GLUT1 and GLUT3. In addition, GLUT8 is expressed in some regions of the brain. By in situ hybridization we detected GLUT8-mRNA in hippocampus, thalamus, and cortex. However, its cellular and physiological function is still unknown. Thus, GLUT8 knockout (Slc2a8
−/−) mice were used for a screening approach in the modified hole board (mHB) behavioral test to analyze the role of GLUT8 in the central nervous system. Slc2a8
−/− mice showed increased mean velocity, total distance traveled and performed more turns in the mHB test. This hyperactivity of Slc2a8
−/− mice was confirmed by monitoring locomotor activity in the home cage and voluntary activity in a running wheel. In addition, Slc2a8
−/− mice showed increased arousal as indicated by elevated defecation, reduced latency to the first defecation and a tendency to altered grooming. Furthermore, the mHB test gave evidence that Slc2a8
−/− mice exhibit a reduced risk assessment because they performed less rearings in an unprotected area and showed significantly reduced latency to stretched body posture. Our data suggest that behavioral alterations of Slc2a8
−/− mice are due to dysfunctions in neuronal processes presumably as a consequence of defects in the glucose metabolism.
TL;DR: The first genome-wide association (GWA) analysis of an environmental measure, called CHAOS, which assesses ‘environmental confusion’ in the home, a measure that is more strongly associated with cognitive development in childhood than any other environmental measure.
Abstract: Widely used measures of the environment, especially the family environment of children, show genetic influence in dozens of twin and adoption studies. This phenomenon is known as gene-environment correlation in which genetically driven influences of individuals affect their environments. We conducted the first genome-wide association (GWA) analysis of an environmental measure. We used a measure called CHAOS which assesses ‘environmental confusion’ in the home, a measure that is more strongly associated with cognitive development in childhood than any other environmental measure. CHAOS was assessed by parental report when the children were 3 years and again when the children were 4 years; a composite CHAOS measure was constructed across the 2 years. We screened 490,041 autosomal single-nucleotide polymorphisms (SNPs) in a two-stage design in which children in low chaos families (N = 469) versus high chaos families (N = 369) from 3,000 families of 4-year-old twins were screened in Stage 1 using pooled DNA. In Stage 2, following SNP quality control procedures, 41 nominated SNPs were tested for association with family chaos by individual genotyping an independent representative sample of 3,529. Despite having 99% power to detect associations that account for more than 0.5% of the variance, none of the 41 nominated SNPs met conservative criteria for replication. Similar to GWA analyses of other complex traits, it is likely that most of the heritable variation in environmental measures such as family chaos is due to many genes of very small effect size.
TL;DR: This is the first study that shows that single individuals specialized in guarding also may have a lower response threshold for stinging, and fits a model of division of labor based on differences in response thresholds to stimuli among workers of different genotypes and task groups that result in non-additive effects on colony behavior.
Abstract: This study was conducted to analyze the stinging response thresholds of individual European and Africanized worker honeybees (Apis mellifera L.) to electrical stimulation. Newly emerged workers were identified, and either were placed into an incubator, into their natal colonies, or cross-fostered in common colonies of European or Africanized ancestry. Nest and guard bees of each type were collected and exposed to an electric stimulus of 0.5 mA, and the time they took to sting a leather substrate was recorded. Africanized bees consistently had significant lower thresholds of defensive response than European bees across all of the environments tested. Guards were faster to sting than nest bees only for the Africanized genotype, suggesting that alleles of African origin have pleiotropic effects on guarding and stinging. This is the first study that shows that single individuals specialized in guarding also may have a lower response threshold for stinging. Environmental effects were also evident. In all cases, bees responded faster to the electrical stimulation after being kept in environments other than their natal nest. Moreover, significant genotype by environment and genotype by task specialization interactions were found. Our results fit a model of division of labor based on differences in response thresholds to stimuli among workers of different genotypes and task groups that result in non-additive effects on colony behavior.
TL;DR: The linkage analyses of NWR in dyslexia provide suggestive and reproducible evidence for linkage to 4p12 and 12p in both samples, and significant evidence for links to 17q in one of the samples.
Abstract: To understand the genetic architecture of dyslexia and identify the locations of genes involved, we performed linkage analyses in multigenerational families using a phonological memory phenotype—Nonword Repetition (NWR). A genome scan was first performed on 438 people from 51 families (DS-1) and linkage was assessed using variance components (VC), Bayesian oligogenic (BO), and parametric analyses. For replication, the genome scan and analyses were repeated on 693 people from 93 families (DS-2). For the combined set (DS-C), analyses were performed with all three methods in the regions that were identified in both samples. In DS-1, regions on chromosomes 4p, 6q, 12p, 17q, and 22q exceeded our initial threshold for linkage, with 17q providing a parametric LOD score of 3.2. Analysis with DS-2 confirmed the locations on chromosomes 4p and 12p. The strongest VC and BO signals in both samples were on chromosome 4p in DS-C, with a parametric multipoint LODmax of 2.36 for the 4p locus. Our linkage analyses of NWR in dyslexia provide suggestive and reproducible evidence for linkage to 4p12 and 12p in both samples, and significant evidence for linkage to 17q in one of the samples. These results warrant further studies of phonological memory and chromosomal regions identified here in other datasets.
TL;DR: Exact data simulation is presented as a third method of power calculation that involves a transformation of raw data so that the data fit the hypothesized model exactly, and is applied to three genetic designs for illustrative purposes.
Abstract: Statistical power calculations constitute an essential first step in the planning of scientific studies. If sufficient summary statistics are available, power calculations are in principle straightforward and computationally light. In designs, which comprise distinct groups (e.g., MZ & DZ twins), sufficient statistics can be calculated within each group, and analyzed in a multi-group model. However, when the number of possible groups is prohibitively large (say, in the hundreds), power calculations on the basis of the summary statistics become impractical. In that case, researchers may resort to Monte Carlo based power studies, which involve the simulation of hundreds or thousands of replicate samples for each specified set of population parameters. Here we present exact data simulation as a third method of power calculation. Exact data simulation involves a transformation of raw data so that the data fit the hypothesized model exactly. As in power calculation with summary statistics, exact data simulation is computationally light, while the number of groups in the analysis has little bearing on the practicality of the method. The method is applied to three genetic designs for illustrative purposes.