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Genetic inheritance is not the only way parents’ genes may affect children. It is also possible that parents’ genes are associated with investments into children’s development. We examined evidence for links between parental genetics and parental investments, from the prenatal period through to adulthood, using data from six population-based cohorts in the UK, US and New Zealand, together totalling 36,566 parents. Our findings revealed associations between parental genetics—summarized in a genome-wide polygenic score—and parental behaviour across development, from smoking in pregnancy, breastfeeding in infancy, parenting in childhood and adolescence, to leaving a wealth inheritance to adult children. Effect sizes tended to be small at any given time point, ranging from RR = 1.12 (95% confidence interval (95%CI) 1.09, 1.15) to RR = 0.76 (95%CI 0.72, 0.80) during the prenatal period and infancy; β = 0.07 (95%CI 0.04, 0.11) to β = 0.29 (95%CI 0.27, 0.32) in childhood and adolescence, and RR = 1.04 (95%CI 1.01, 1.06) to RR = 1.11 (95%CI 1.07, 1.15) in adulthood. There was evidence for accumulating effects across development, ranging from β = 0.15 (95%CI 0.11, 0.18) to β = 0.23 (95%CI 0.16, 0.29) depending on cohort. Our findings are consistent with the interpretation that parents pass on advantages to offspring not only via direct genetic transmission or purely environmental paths, but also via genetic associations with parental investment from conception to wealth inheritance.

Social interactions among animals can be complex, and abnormal social behaviours may result in negative fitness consequences for both the individual displaying them, and the entire group. To understand the neural basis of complex social behaviour, we can study simpler behaviours that precede and mediate them. Social spacing, the typical distance between individuals in a group, is an easily quantifiable behaviour in Drosophila melanogaster. Here, I investigated the neural circuitry underlying social spacing through the lens of Autism-candidate gene neuroligin 3. Based on the Nlg3 enrichment pattern in adult fly brains, I hypothesized that nlg3-expressing neurons, along with the mushroom bodies and protocerebral bridge, were involved in this behaviour. I determined that all the aforementioned structures are involved, and there is likely sexual dimorphism in this neural circuitry. This research contributes to understanding the role Nlg3 plays in social spacing and reveals more routes of neural connectivity to be investigated.

BACKGROUND: The philosophical debate about the roles of nature versus nurture in human flourishing is not new. But the rise of precision education—a growing field of research that encourages the use of genetic data to inform educational interventions to better meet student needs—has renewed historical and ethical concerns. A major worry is that “genetic hype” may skew public perceptions toward a deterministic perception of the child’s educational trajectory, regardless of the child’s capacities, and underestimation of environmental factors affecting educational outcomes. We tested this hypothesis with parents and adults from the general public in the US. METHODS: A newly developed computerized implicit association test (IAT) to assess automatic associations between genetics or environments and student behaviors that are associated with educational achievement was administered to samples of parents of children below 21 years old (n=450) and adults from the general public (n=419). The samples were representative of the adult US population and adjusted to oversample Black/African American participants. An overall D score for participants’ IATs (range: [−2, 2]) was calculated on the basis of the speed of participants’ responses. RESULTS: The mean IAT score for both samples indicated stronger association between the quality of being a good student and environment rather than genetics (parents: mean=−0.146, t=−6.56, p

Understanding underlying genetic variation can elucidate how diversity in behavioral phenotypes evolves and is maintained. Genes in the serotonergic signaling pathway, including the serotonin transporter gene (SERT), are candidates for affecting animal personality, cognition and fitness. In a model species, the great tit (Parus major), we reevaluated previous findings suggesting relationships between SERT polymorphisms, neophobia, exploratory behavior and fitness parameters, and performed a first test of the relationship between single nucleotide polymorphisms (SNPs) in SERT and problem-solving in birds. We found some evidence for associations between SERT SNPs and neophobia, exploratory behavior and laying date. Furthermore, several SNPs were associated with behavioral patterns and success rates during obstacle removal problem-solving tests performed at nest boxes. In females, minor allele homozygotes (AA) for nonsynonymous SNP226 in exon 1 made fewer incorrect attempts and were more likely to problem-solve. In both sexes, there was some evidence that minor allele homozygotes (CC) for SNP84 in exon 9 were more likely to problem-solve. Only one SNP-behavior relationship was statistically significant after correcting for multiple comparisons, but several were associated with substantial effect sizes. Our study provides a foundation for future research on the genetic basis of behavioral and cognitive variation in wild animal populations.

Peer reviewed: True, Funder: NIHR Cambridge Biomedical Research Centre; FundRef: https://doi.org/10.13039/501100018956, Funder: Autism Research Trust, Funder: Autistica; FundRef: https://doi.org/10.13039/501100008161, Funder: Templeton World Charity Foundation; FundRef: https://doi.org/10.13039/501100011730, Funder: NIHR Collaboration for Leadership in Applied Health Research and Care East of England at Cambridgeshire and Peterborough NHS Foundation Trust, Funder: Medical Research Council; FundRef: https://doi.org/10.13039/501100000265, Assortative mating is a phenomenon in which romantic partners typically resemble each other at a level greater than chance. There is converging evidence that social behaviours are subject to assortative mating, though less is known regarding social cognition. Social functioning requires the ability to identify and understand the mental states of others, i.e., theory of mind. The present study recruited a sample of 102 heterosexual couples via an online survey to test if theory of mind as measured using facial expressions (Reading the Mind in the Eyes Test) or language (Stiller-Dunbar Stories Task) is associated with assortative mating. Results provide evidence of assortative mating for theory of mind via facial expressions, though there was no such effect for theory of mind via language. Assortative mating for theory of mind via facial expressions was not moderated by length of relationship nor by partner similarity in age, educational attainment, or religiosity, all variables relevant to social stratification. This suggests assortative mating for theory of mind via facial expressions is better explained by partners being alike at the start of their relationship (initial assortment) rather than becoming similar through sustained social interaction (convergence), and by people seeking out partners that are like themselves (active assortment) rather than simply pairing with those from similar demographic backgrounds (social homogamy).

Attention Deficit-Hyperactivity Disorder (ADHD) is a complex psychiatric and neurodevelopmental disorder that develops during childhood and spans into adulthood. ADHD’s aetiology is complex, and evidence about its cause and risk factors is limited. We leveraged genetic data from genome-wide association studies (GWAS) and performed latent causal variable analyses using a hypothesis-free approach to infer causal associations between 1387 complex traits and ADHD. We identified 37 inferred potential causal associations with ADHD risk. Our results reveal that genetic variants associated with iron deficiency anemia (ICD10), obesity, type 2 diabetes, synovitis and tenosynovitis (ICD10), polyarthritis (ICD10), neck or shoulder pain, and substance use in adults display partial genetic causality on ADHD risk in children. Genetic variants associated with ADHD have a partial genetic causality increasing the risk for chronic obstructive pulmonary disease and carpal tunnel syndrome. Protective factors for ADHD risk included genetic variants associated with the likelihood of participating in socially supportive and interactive activities. Our results show that genetic liability to multiple complex traits influences a higher risk for ADHD, highlighting the potential role of cardiometabolic phenotypes and physical pain in ADHD’s aetiology. These findings have the potential to inform future clinical studies and development of interventions.

BackgroundRecent well-powered genome-wide association studies have enhanced prediction of substance use outcomes via polygenic scores (PGSs). Here, we test (1) whether these scores contribute to prediction over-and-above family history, (2) the extent to which PGS prediction reflects inherited genetic variation v. demography (population stratification and assortative mating) and indirect genetic effects of parents (genetic nurture), and (3) whether PGS prediction is mediated by behavioral disinhibition prior to substance use onset.MethodsPGSs for alcohol, cannabis, and nicotine use/use disorder were calculated for Minnesota Twin Family Study participants (N = 2483, 1565 monozygotic/918 dizygotic). Twins' parents were assessed for histories of substance use disorder. Twins were assessed for behavioral disinhibition at age 11 and substance use from ages 14 to 24. PGS prediction of substance use was examined using linear mixed-effects, within-twin pair, and structural equation models.ResultsNearly all PGS measures were associated with multiple types of substance use independently of family history. However, most within-pair PGS prediction estimates were substantially smaller than the corresponding between-pair estimates, suggesting that prediction is driven in part by demography and indirect genetic effects of parents. Path analyses indicated the effects of both PGSs and family history on substance use were mediated via disinhibition in preadolescence.ConclusionsPGSs capturing risk of substance use and use disorder can be combined with family history measures to augment prediction of substance use outcomes. Results highlight indirect sources of genetic associations and preadolescent elevations in behavioral disinhibition as two routes through which these scores may relate to substance use.

The field of human behavioral genetics has come full circle. It began by using twin/family studies to estimate the relative importance of genetic and environmental influences. As large-scale genotyping became cost-effective, genome-wide association studies (GWASs) yielded insights about the nature of genetic influences, and new methods that use GWAS data to estimate heritability and genetic correlations invigorated the field. Yet these newer GWAS methods have not replaced twin/family studies. In this review, we discuss the strengths and weaknesses of the two approaches with respect to characterizing genetic and environmental influences, measurement of behavioral phenotypes, and evaluation of causal models, with a particular focus on cognitive neuroscience. This discussion highlights how twin/family studies and GWAS complement and mutually reinforce one another.

The ability to characterize muscle activities or skilled movements controlled by signals from neurons in the motor cortex of the brain has many useful implications, ranging from biomedical perspectives to brain–computer interfaces. This paper presents the method of recurrence eigenvalues for differentiating moving patterns in non-mammalian and human models. The non-mammalian models of Caenorhabditis elegans have been studied for gaining insights into behavioral genetics and discovery of human disease genes. Systematic probing of the movement of these worms is known to be useful for these purposes. Study of dynamics of normal and mutant worms is important in behavioral genetic and neuroscience. However, methods for quantifying complexity of worm movement using time series are still not well explored. Neurodegenerative diseases adversely affect gait and mobility. There is a need to accurately quantify gait dynamics of these diseases and differentiate them from the healthy control to better understand their pathophysiology that may lead to more effective therapeutic interventions. This paper attempts to explore the potential application of the method for determining the largest eigenvalues of convolutional fuzzy recurrence plots of time series for measuring the complexity of moving patterns of Caenorhabditis elegans and neurodegenerative disease subjects. Results obtained from analyses demonstrate that the largest recurrence eigenvalues can differentiate phenotypes of behavioral dynamics between wild type and mutant strains of Caenorhabditis elegans; and walking patterns among healthy control subjects and patients with Parkinson’s disease, Huntington’s disease, or amyotrophic lateral sclerosis.

Sleep is a fundamental behavioral state important for survival and is universal in animals with sufficiently complex nervous systems. As a highly conserved neurobehavioral state, sleep has been described in species ranging from jellyfish to humans. Biogenic amines like dopamine, serotonin and norepinephrine have been shown to be critical for sleep regulation across species but the precise circuit mechanisms underlying how amines control persistence of sleep, arousal and wakefulness remain unclear. The fruit fly, Drosophila melanogaster, provides a powerful model system for the study of sleep and circuit mechanisms underlying state transitions and persistence of states to meet the organisms motivational and cognitive needs. In Drosophila, two neuropils in the central brain, the mushroom body (MB) and the central complex (CX) have been shown to influence sleep homeostasis and receive aminergic neuromodulator input critical to sleep–wake switch. Dopamine neurons (DANs) are prevalent neuromodulator inputs to the MB but the mechanisms by which they interact with and regulate sleep- and wake-promoting neurons within MB are unknown. Here we investigate the role of subsets of PAM-DANs that signal wakefulness and project to wake-promoting compartments of the MB. We find that PAM-DANs are GABA responsive and require GABAA-Rdl receptor in regulating sleep. In mapping the pathways downstream of PAM neurons innervating γ5 and β′2 MB compartments we find that wakefulness is regulated by both DopR1 and DopR2 receptors in downstream Kenyon cells (KCs) and mushroom body output neurons (MBONs). Taken together, we have identified and characterized a dopamine modulated sleep microcircuit within the mushroom body that has previously been shown to convey information about positive and negative valence critical for memory formation. These studies will pave way for understanding how flies balance sleep, wakefulness and arousal.

This brief communication responds to the article by Rajabi et al., recently published in Behavior Genetics. To test the hypothesis of cigarette smoking as a "gateway" for subsequent opium use and contrast it with the common liability model, Mendelian randomization analysis was applied to data obtained from an Iranian sample, using CHRNA3 rs1051730 as an instrumental variable. It is doubtful, however, if the assumptions of instrumental variable analysis hold in this case. The authors misstate both the gateway hypothesis and the common liability model. The article has many other deficiencies that diminish the veracity of its categorical conclusions that accept the causal interpretation of the "gateway hypothesis" and reject the common liability model, with which the data are fully consistent.

Based on the analysis of the content of the book of famous British behavioral geneticists K. Asbury and R. Plomin «G means genes: the impact of genetics on education and achievement» shows the way to create a perfect school education, based on the latest numerous large-scale and long-term researches in different countries and prove that the role of genetic factors in human learning and life success is not absolute and that the impact of the environment is no less important than genes. This thesis is a base of the personalized child education idea. Based on an analysis of the research results, the authors of the book assert that school education should be personalized. It is the personalization of learning that will ensure to develop the thinking ability, acquire knowledge and skills at a pace and direction that is appropriate for each child. Personalized learning should be based on the following principles: a minimization of the core curriculum and test basic knowledge and skills; a maximizing of options to all pupils alongside the compulsory basic knowledge and skills; a stopping of labeling ability of children; an individual education of each pupil; a teaching of children to achieve success; a promotion of equal opportunities for children from an early age; an availability of out-of-school education for all children; a two-stage physical education program; wide choice of future life ways; a training of new teachers in genetics and a giving them the methods to put it into pedagogical practice; the scale of schools in directions and levels of education. Finally, the authors of the book offer their vision of a school that will be based on the laws of behavioral genetics. Possible publication of the book by K. Asbury and R. Plomin, «G is for genes: The impact of genetics on education and achievement» in Ukrainian will be an interesting and useful handbook for policymakers, educators and parents with its constructive recommendations on one of the most important educational challenges – how to prepare each and every child for a successful life in today's ever-changing world.

As exemplified by the Ebbinghaus illusion, the perceived size of an object can be significantly biased by its surrounding context. The phenomenon is experienced by humans as well as other species, hence likely evolutionarily adaptive. Here, we examined the heritability of the Ebbinghaus illusion using a combination of the classic twin method and multichannel functional near-infrared spectroscopy. Results show that genes account for over 50% of the variance in the strength of the experienced illusion. Interestingly, activations evoked by the Ebbinghaus stimuli in the early visual cortex are explained by genetic factors whereas those in the posterior temporal cortex are explained by environmental factors. In parallel, the feedforward functional connectivity between the occipital cortex and the temporal cortex is modulated by genetic effects whereas the feedback functional connectivity is entirely shaped by environment, despite both being significantly correlated with the strength of the experienced illusion. These findings demonstrate that genetic and environmental factors work in tandem to shape the context-dependent visual size illusion, and shed new light on the links among genes, environment, brain, and subjective experience.

Введение. Представленный научный обзор направлен на понимание этиологии пространственных способностей человека. Пространственное мышление – сложный комплекс когнитивных способностей, позволяющих распознавать, преобразовывать и сохранять информацию об объектах, прогнозировать трансформацию взаимодействий между ними под влиянием прочих факторов. Настоящая работа направлена на получение наиболее полного описания пространственных способностей как специфического вида умственной деятельности, лежащего в основе выполнения практических и теоретических задач, решаемых индивидом, с позиции психологии и генетики, чтобы подчеркнуть важность синтеза накопленных экспериментальных данных и психологических основ пространственного интеллекта в общем. Теоретическое обоснование. Представлен обзор результатов генетически информативных исследований пространственных способностей человека. Так как умение ориентироваться в пространстве является неотъемлемой чертой всех живых организмов, пространственные способности имеют эволюционно-адаптивное значение и также важны для индивида. В когнитивной психологии под пространственными навыками понимаются способности оперировать мысленными пространственными образами, схемами, моделями реальности, причем эти способности существенно различаются между людьми. Анализ этиологии этих индивидуальных различий выявил значительный вклад (69 %) наследственных факторов в формирование пространственных способностей. Результаты близнецовых исследований ставят задачу поиска конкретных полиморфных вариантов в генах, вовлеченных в развитие пространственных навыков. В целом ряде масштабных лонгитюдных исследований показано, что пространственные способности являются надежным предиктором достижений человека в области естественных наук, технологий, инженерии и математики (STEM), поэтому изучение их молекулярно-генетических механизмов представляется важной и актуальной задачей. Результаты и их обсуждение. В ходе проведения различного рода экспериментальных работ по психогенетике пространственных способностей человека были впервые получены весьма интересные данные, подтверждающие их наследственную природу. Выявлено, что пространственный интеллект является умеренно наследуемым признаком, в развитии которого задействован широкий спектр генетических факторов, обуславливающих активацию различных сигнальных путей метаболизма организма человека.

Naltrexone can aid in reducing alcohol consumption, while acamprosate supports abstinence; however, not all patients with alcohol use disorder (AUD) benefit from these treatments. Here we present the first genome-wide association study of AUD treatment outcomes based on data from the COMBINE and PREDICT studies of acamprosate and naltrexone, and the Mayo Clinic CITA study of acamprosate. Primary analyses focused on treatment outcomes regardless of pharmacological intervention and were followed by drug-stratified analyses to identify treatment-specific pharmacogenomic predictors of acamprosate and naltrexone response. Treatment outcomes were defined as: (1) time until relapse to any drinking (TR) and (2) time until relapse to heavy drinking (THR; ≥ 5 drinks for men, ≥4 drinks for women in a day), during the first 3 months of treatment. Analyses were performed within each dataset, followed by meta-analysis across the studies (N = 1083 European ancestry participants). Single nucleotide polymorphisms (SNPs) in the BRE gene were associated with THR (min p = 1.6E−8) in the entire sample, while two intergenic SNPs were associated with medication-specific outcomes (naltrexone THR: rs12749274, p = 3.9E−8; acamprosate TR: rs77583603, p = 3.1E−9). The top association signal for TR (p = 7.7E−8) and second strongest signal in the THR (p = 6.1E−8) analysis of naltrexone-treated patients maps to PTPRD, a gene previously implicated in addiction phenotypes in human and animal studies. Leave-one-out polygenic risk score analyses showed significant associations with TR (p = 3.7E−4) and THR (p = 2.6E−4). This study provides the first evidence of a polygenic effect on AUD treatment response, and identifies genetic variants associated with potentially medication-specific effects on AUD treatment response.

The WMI and WLI inbred rats were generated from the stress-prone, and not yet fully inbred, Wistar Kyoto (WKY) strain. These were selected using bi-directional selection for immobility in the forced swim test and were then sib-mated for over 38 generations. Despite the low level of genetic diversity among WKY progenitors, the WMI substrain is significantly more vulnerable to stress relative to the counter-selected WLI strain. Here we quantify numbers and classes of genomic sequence variants distinguishing these substrains with the long term goal of uncovering functional and behavioral polymorphism that modulate sensitivity to stress and depression-like phenotypes. DNA from WLI and WMI was sequenced using Illumina xTen, IonTorrent, and 10X Chromium linked-read platforms to obtain a combined coverage of ~ 100X for each strain. We identified 4,296 high quality homozygous SNPs and indels between the WMI and WLI. We detected high impact variants in genes previously implicated in depression (e.g. Gnat2), depression-like behavior (e.g. Prlr, Nlrp1a), other psychiatric disease (e.g. Pou6f2, Kdm5a, Reep3, Wdfy3), and responses to psychological stressors (e.g. Pigr). High coverage sequencing data confirm that the two substrains are nearly coisogenic. Nonetheless, the small number of sequence variants contributes to numerous well characterized differences including depression-like behavior, stress reactivity, and addiction related phenotypes. These selected substrains are an ideal resource for forward and reverse genetic studies using a reduced complexity cross.

Many behavior genetics models follow the same general structure. We describe this general structure and analytically derive simple criteria for its identification. In particular, we find that variance components can be uniquely estimated whenever the relatedness matrices that define the components are linearly independent (i.e., not confounded). Thus, we emphasize determining which variance components can be identified given a set of genetic and environmental relationships, rather than the estimation procedures. We validate the identification criteria with several well-known models, and further apply them to several less common models. The first model distinguishes child-rearing environment from extended family environment. The second model adds a gene-by-common-environment interaction term in sets of twins reared apart and together. The third model separates measured-genomic relatedness from the scanner site variation in a hypothetical functional magnetic resonance imaging study. The computationally easy analytic identification criteria allow researchers to quickly address model identification issues and define novel variance components, facilitating the development of new research questions.

Trajectories of youth antisocial behavior (ASB) are characterized by both continuity and change. Twin studies have further indicated that genetic factors underlie continuity, while environmental exposures unique to each child in a given family underlie change. However, most behavioral genetic studies have examined continuity and change during relatively brief windows of development (e.g., during childhood but not into adolescence). It is unclear whether these findings would persist when ASB trajectories are examined across multiple stages of early development (i.e., from early childhood into emerging adulthood). Our study sought to fill this gap by examining participants assessed up to five times between the ages of 3 and 22 years using an accelerated longitudinal design in the Michigan State University Twin Registry (MSUTR). We specifically examined the etiologies of stability and change via growth curve modeling and a series of univariate and bivariate twin analyses. While participants exhibited moderate-to-high rank-order stability, mean levels of ASB decreased linearly with age. Genetic and nonshared environmental influences that were present in early childhood also contributed to both stability and change across development, while shared environmental contributions were negligible. In addition, genetic and nonshared environmental influences that were not yet present at the initial assessment contributed to change over time. Although ASB tended to decrease in frequency with age, participants who engaged in high levels of ASB during childhood generally continued to do so throughout development. Moreover, the genetic and nonshared environmental contributions to ASB early in development also shaped the magnitude of the decrease with age.

Alcohol-related physical violence (ARPV) can be a causal consequence of alcohol consumption, but only for specific individuals (e.g., those predisposed to violence). Studies have not accounted for the shared etiology explaining comorbidity between alcohol use and violent behavior as a potential third-variable explanation of ARPV. The current study examined genetically-informed associations between ARPV, heavy alcohol use (HAU) and overall physical violence (OPV) in adolescence and young adulthood, by testing two proposed theories of ARPV processes (HAU causes ARPV, causal relationships depend upon OPV) and how overarching shared covariance may account for these associations.Using the twin and sibling subsample from the National Longitudinal Study of Adolescent to Adult Health (Add Health), a series of biometric models tested hypotheses individually in adolescence and young adulthood. This included estimating bivariate Cholesky and direction-of-causality models, and trivariate Cholesky, independent pathway, and common pathway models.HAU had a causal effect on ARPV in adolescence and young adulthood. This effect was not moderated by OPV at either developmental stage. A shared etiology or common latent factor did not explain associations between ARPV, OPV, and HAU, even though ARPV strongly covaried independently with HAU and with OPV. Finally, OPV also had a causal effect on ARPV in adolescence, and in young adulthood for adolescent-onset drinkers.Causal theories of ARPV still hold when accounting for shared genetic and environmental variance. Further research on the exact role of violence (predispositions, environmental contexts) is required, as both phenotypes substantially (and separately) explain influences driving ARPV.Supplemental data for this article is available online at https://doi.org/10.1080/10826084.2021.1887244.

Parents with substance misuse provide their children with a potentially risky rearing environment. According to the evolutionary life history theory, such environments steer individuals towards faster reproductive strategy. However, parents providing their children with hazardous environments may also pass on genes associated with early parenthood. In register data on individuals born in Sweden 1973–1993 (N = 2,176,128), the hazard ratio of entering parenthood by age 25 was 1.70 (95% CI 1.69–1.72) and 1.85 (1.82–1.89) among offspring of fathers and mothers with substance misuse, respectively, compared to others. In analyses using an offspring-of-siblings design in three types of parental sibling pairs (half siblings, full siblings and dizygotic twins, and monozygotic twins) increasingly controlling for genetic confounding, associations between parental substance misuse and offspring's early reproduction gradually attenuated. Our results suggest that the association between parental substance misuse and earlier parenthood in offspring is at least partly genetically confounded. Life history theory should be further tested with genetically informative research designs.

Autism spectrum disorder is associated with sensory processing alterations, such as sensory hyper- and hypo-responsiveness. Twin studies are scarce in this field, but they are necessary in order to disentangle the genetic and environmental contributions to this association. Furthermore, it is unclear how different neurodevelopmental/psychiatric conditions contribute to altering sensory processing. We investigated the association between autistic traits/autism spectrum disorder diagnosis and sensory processing alterations in twins ( N = 269), using the adult/adolescent sensory profile, which differentiates four sub-domains: Low Registration, Sensation Seeking, Sensory Sensitivity, and Sensation Avoiding. While the associations between autistic traits and Low Registration and Sensation Avoiding persisted within monozygotic (genetically identical) twins, Sensory Sensitivity was only associated with autistic traits within dizygotic twins. In multivariate analyses with different neurodevelopmental/psychiatric diagnoses as predictor variables, autism spectrum disorder and attention deficit hyperactivity disorder were the strongest predictors for two adult/adolescent sensory profile sub-domains each. The results suggest that the association between autistic traits and Sensory Sensitivity is influenced by genetics while non-shared environmental factors influence the associations between autistic traits and Low Registration and Sensation Avoiding. They further indicate that altered sensory processing is not specific to autism spectrum disorder, while autism spectrum disorder is a strong predictor of certain sensory processing alterations, even when controlling for other (comorbid) neurodevelopmental/psychiatric conditions. Lay abstract Individuals diagnosed with autism often describe that they process sensory information differently from others, and many experience sensory issues as problematic. For instance, an increased sensitivity to smells or sounds can make participating in social settings challenging. While sensory issues are now part of the diagnostic criteria for autism, they also co-occur with other psychiatric diagnoses such as attention deficit hyperactivity disorder and anxiety disorders. It is unclear to what extent the relationship between autism and alterations in sensory processing are due to genetics or environment. In addition, more research is needed on how autism, as compared to other diagnoses, is associated with sensory issues. Using a twin study, we found that genetic factors influenced self-reported reactivity to sensory stimuli in autism while environmental factors influenced other sensory issues (e.g. difficulties in detecting or differentiating sensory input). Hence, sensory hyper-reactivity might be an early onset core feature of autism, while other domains of alterations in sensory processing might develop later, influenced by the environment. Moreover, autism was more strongly associated with sensory issues related to increased sensitivity/reactivity as compared to other psychiatric diagnoses. However, attention deficit hyperactivity disorder was more strongly related to deficits in detecting/differentiating sensory stimuli and with an increased drive to seek sensory input. Our results indicate that sensory issues are not specific to autism, but that some aspects of altered sensory processing are more relevant for autism than for other diagnoses.

Here we introduce ‘FAQs on Genomic Studies’ (FoGS), an open-access repository of explanatory documents that accompany genomic analyses in social and behavioral genomics. For fields such as social and behavioral genomics that are shaped by an ugly history and uncertain future, socially and ethically responsible research and research communication are crucial. FoGS amplifies one such approach towards responsible research communication.

For more than a decade, it has been known that many common behavior genetics models for a single phenotype can be estimated as multilevel models (e.g., van den Oord 2001; Guo and Wang 2002; McArdle and Prescott 2005; Rabe-Hesketh et al. 2007). This paper extends the current knowledge to (1) multiple phenotypes such that the method is completely general to the variance structure hypothesized, and (2) both higher and lower levels of nesting. The multi-phenotype method also allows extended relationships to be considered (see also, Bard et al. 2012; Hadfield and Nakagawa 2010). The extended relationship model can then be continuously expanded to merge with the case typically seen in the molecular genetics analyses of unrelated individuals (e.g., Yang et al. 2011). We use the multilevel form of behavior genetics models to fit a multivariate three level model that allows for (1) child level variation from unique environments and additive genetics, (2) family level variation from additive genetics and common environments, and (3) neighborhood level variation from broader geographic contexts. Finally, we provide R (R Development Core Team 2020) functions and code for multilevel specification of several common behavior genetics models using OpenMx (Neale et al. 2016).

Introduction Electronic cigarettes are now the most commonly used form of tobacco product among youth in the United States. Current evidence suggests that although e-cigarettes are perceived as less harmful and preferred over combustible cigarettes by adolescents, adolescents who try e-cigarettes are at greater risk of transitioning to combustible cigarettes. The genetic and environmental contributions to liability for e-cigarette use have not yet been examined using a behavioral genetic design. Methods Behavioral genetic models of lifetime and current e-cigarette use and friends who use e-cigarettes were examined among female monozygotic and dizygotic twins. Results A total of 41 female twin pairs (65.9% monozygotic twins; age = 19.7, SD = 1.6) with complete data on the study variables were included in the present analyses. The majority of the sample (68.1%) had at least some friends who use e-cigarettes. Additive genetic effects on e-cigarette use were not present, but the shared environment explained 98.7% of the variance in lifetime e-cigarette use, 96.6% in current e-cigarette use, and 94.9% in affiliation with friends who use e-cigarettes. Conclusion This first study on the behavioral genetics of e-cigarette use among adolescents and young adults suggest that environmental factors shared by twins within a family seem to play a predominant role in the initial stages of e-cigarette use, a finding that is consistent with what has been found for tobacco. The findings emphasize the importance of continuing population-based tobacco control interventions to reduce the burden of e-cigarette use among adolescents. Implications The shared environment significantly influences the initiation and regular use of electronic cigarettes and affiliation with friends who use electronic cigarettes among adolescent and young adult females. These findings underscore the importance of formulating preventive interventions that mitigate the social effects of familial influences on e-cigarette use through social skills training, education on harms of e-cigarettes for young people, or altering social norms regarding initiation of novel tobacco products.

The nematode C. elegans is a leading model to investigate the mechanisms of stress-induced behavioral changes coupled with biochemical mechanisms. Our group has previously characterized C. elegans behavior using a microfluidic-based electrotaxis device, and showed that worms display directional motion in the presence of a mild electric field. In this study, we describe the effects of various forms of genetic and environmental stress on the electrotactic movement of animals. Using exposure to chemicals, such as paraquat and tunicamycin, as well as mitochondrial and endoplasmic reticulum (ER) unfolded protein response (UPR) mutants, we demonstrate that chronic stress causes abnormal movement. Additionally, we report that pqe-1 (human RNA exonuclease 1 homolog) is necessary for the maintenance of multiple stress response signaling and electrotaxis behavior of animals. Further, exposure of C. elegans to several environmental stress-inducing conditions revealed that while chronic heat and dietary restriction caused electrotaxis speed deficits due to prolonged stress, daily exercise had a beneficial effect on the animals, likely due to improved muscle health and transient activation of UPR. Overall, these data demonstrate that the electrotaxis behavior of worms is susceptible to cytosolic, mitochondrial, and ER stress, and that multiple stress response pathways contribute to its preservation in the face of stressful stimuli.

Many animals use the Earth’s geomagnetic field for orientation and navigation. Yet, the molecular and cellular underpinnings of the magnetic sense remain largely unknown. A biophysical model proposed that magnetoreception can be achieved through quantum effects of magnetically-sensitive radical pairs formed by the photoexcitation of cryptochrome (CRY) proteins. Studies in Drosophila are the only ones to date to have provided compelling evidence for the ultraviolet (UV)-A/blue light-sensitive type 1 CRY (CRY1) involvement in animal magnetoreception, and surprisingly extended this discovery to the light-insensitive mammalian-like type 2 CRYs (CRY2s) of both monarchs and humans. Here, we show that monarchs respond to a reversal of the inclination of the Earth’s magnetic field in an UV-A/blue light and CRY1, but not CRY2, dependent manner. We further demonstrate that both antennae and eyes, which express CRY1, are magnetosensory organs. Our work argues that only light-sensitive CRYs function in animal light-dependent inclination-based magnetic sensing., Exactly how some animals use magnetic fields to navigate is a longstanding puzzle. A study using a new behavioural assay and transgenic butterflies finds the cryptochrome gene necessary for inclination-based magnetic sensing, and shows that both antennae and eyes, which express this gene, are magnetosensory organs.

How well one does at school is predictive of a wide range of important cognitive, socioeconomic, and health outcomes. The last few years have shown marked advancement in our understanding of the genetic contributions to, and correlations with, academic attainment. However, there exists a gap in our understanding of the specificity of genetic associations with performance in academic subjects during adolescence, a critical developmental period. To address this, the Avon Longitudinal Study of Parents and Children was used to conduct genome-wide association studies of standardised national English (N = 5983), maths (N = 6017) and science (N = 6089) tests. High SNP-based heritabilities (h2SNP) for all subjects were found (41–53%). Further, h2SNP for maths and science remained after removing shared variance between subjects or IQ (N = 3197–5895). One genome-wide significant single nucleotide polymorphism (rs952964, p = 4.86 × 10–8) and four gene-level associations with science attainment (MEF2C, BRINP1, S100A1 and S100A13) were identified. Rs952964 remained significant after removing the variance shared between academic subjects. The findings highlight the benefits of using environmentally homogeneous samples for genetic analyses and indicate that finer-grained phenotyping will help build more specific biological models of variance in learning processes and abilities.