Gene X Environment Interactions

For Ethiopia's wheat production, drought is a major natural disaster. Exploration of drought-resistant varieties from a bulk of wheat germplasm conserved in the gene bank is of paramount importance for breeding climate change-resilient modern cultivars. The present study was aimed at identifying the best performing drought-resistant genotypes under non-stress and polyethylene glycol simulated (PEG) stress conditions in a growth chamber. Forty diverse Ethiopian bread and durum wheat cultivars along with three Chinese bread wheat cultivars possessing strong drought resistance and susceptibility were evaluated. After acclimation with the natural environment, the seedlings were imposed to severe drought stress (20% PEG 6000), and 15 seedling traits including photosynthetic and free proline were investigated. Our findings indicated that drought stress caused a profound decline in plant water consumption (83.0%), shoot fresh weight (64.9%), stomatal conductance (61.6%), root dry weight (55.2%), and other investigated traits except root to shoot length ratio and proline content which showed a significant increase under drought stress. A significant and positive correlation was found between photosynthetic pigments in both growth conditions. Proline exhibited a negative correlation with most of the investigated traits except root to shoot length ratio and all photosynthetic pigments which showed a positive and non-significant association. Our result also showed a wide range of genetic variation (CV) ranging from 3.23% to 47.3%; the highest in shoot dry weight (SDW) (47.3%) followed by proline content (44.63%) and root dry weight (36.03%). Based on multivariate principal component biplot analysis and average sum of ranks (ASR), G12, G16 and G25 were identified as the best drought tolerant and G6, G42, G4, G11, and G9 as bottom five sensitive. The potential of these genotypes offers further investigation at a molecular and cellular level to identify the novel gene associated with the stress response.

SummaryStudies of how genetic and environmental exposures interact may be essential for understanding the aetiology of complex psychiatric disorders. In this issue of the Journal an Australian study reports evidence of such an interaction on risk of depression. We discuss findings in this field in the context of the limitations inherent in studies of gene–environment interactions.

Language development requires both basic cognitive mechanisms for learning language and a rich social context from which learning takes off. Disruptions in learning mechanisms, processing abilities, and/or social interactions increase the risks associated with social exclusion or developmental delays. Given the complexity of language processes, a multilevel approach is proposed where both cognitive mechanisms, genetic and environmental factors need to be probed together with their possible interactions. Here we review and discuss such interplay between environment and genetic predispositions in understanding language disorders, with a particular focus on a possible endophenotype, the ability for statistical sequential learning.

Human language appears to be unique among natural communication systems, and such uniqueness impinges on both nature and nurture. Human babies are endowed with cognitive abilities that predispose them to learn language, and this process cannot operate in an impoverished environment. To be effectively complete the acquisition of human language in human children requires highly socialised forms of learning, scaffolded over years of prolonged and intense caretaker-child interactions. How genes and environment operate in shaping language is unknown. These two components have traditionally been considered as independent, and often pitted against each other in terms of the nature versus nurture debate. This perspective article considers how innate abilities and experience might instead work together. In particular, it envisages potential scenarios for research, in which early caregiver verbal and non-verbal attachment practices may mediate or moderate the expression of human genetic systems for language.

Genome-wide transcription profiling is a powerful technique in studying disease susceptible footprints. Moreover, when applied to disease tissue it may reveal quantitative and qualitative alterations in gene expression that give information on the context or underlying basis for the disease and may provide a new diagnostic approach. However, the data obtained from high-density microarrays is highly complex and poses considerable challenges in data mining. Past researches prove that neuro diseases damage the brain network interaction, protein-protein interaction and gene-gene interaction. A number of neurological research paper also analyze the relationship among damaged part. Analysis of gene-gene interaction network drawn by using state-of-the-art gene database of Alzheimer's patient can conclude a lot of information. In this paper we used gene dataset affected with Alzheimer's disease and normal patient's dataset from NCBI databank. After proper processing the .CEL affymetrix data using RMA, we use the processed data to find gene interaction outputs. Then we filter the output files using probe set filtering attributes p-value and fold count and draw a gene-gene interaction network. Then we analyze the interaction network using GeneMania software.

Genome-wide transcription profiling is a powerful technique in studying disease susceptible footprints. Moreover, when applied to disease tissue it may reveal quantitative and qualitative alterations in gene expression that give information on the context or underlying basis for the disease and may provide a new diagnostic approach. However, the data obtained from high-density microarrays is highly complex and poses considerable challenges in data mining. Past researches prove that neuro diseases damage the brain network interaction, protein-protein interaction and gene-gene interaction. A number of neurological research paper also analyze the relationship among damaged part. Analysis of gene-gene interaction network drawn by using state-of-the-art gene database of Alzheimer's patient can conclude a lot of information. In this paper we used gene dataset affected with Alzheimer's disease and normal patient's dataset from NCBI databank. After proper processing the .CEL affymetrix data using RMA, we use the processed data to find gene interaction outputs. Then we filter the output files using probe set filtering attributes p-value and fold count and draw a gene-gene interaction network. Then we analyze the interaction network using GeneMania software.

Genome-wide transcription profiling is a powerful technique in studying disease susceptible footprints. Moreover, when applied to disease tissue it may reveal quantitative and qualitative alterations in gene expression that give information on the context or underlying basis for the disease and may provide a new diagnostic approach. However, the data obtained from high-density microarrays is highly complex and poses considerable challenges in data mining. Past researches prove that neuro diseases damage the brain network interaction, protein-protein interaction and gene-gene interaction. A number of neurological research paper also analyze the relationship among damaged part. Analysis of gene-gene interaction network drawn by using state-of-the-art gene database of Alzheimer's patient can conclude a lot of information. In this paper we used gene dataset affected with Alzheimer's disease and normal patient's dataset from NCBI databank. After proper processing the .CEL affymetrix data using RMA, we use the processed data to find gene interaction outputs. Then we filter the output files using probe set filtering attributes p-value and fold count and draw a gene-gene interaction network. Then we analyze the interaction network using GeneMania software.

Language development requires both basic cognitive mechanisms for learning language and a rich social context from which learning takes off. Disruptions in learning mechanisms, processing abilities, and/or social interactions increase the risks associated with social exclusion or developmental delays. Given the complexity of language processes, a multilevel approach is proposed where both cognitive mechanisms, genetic and environmental factors need to be probed together with their possible interactions. Here we review and discuss such interplay between environment and genetic predispositions in understanding language disorders, with a particular focus on a possible endophenotype, the ability for statistical sequential learning.

Meta-analytic evidence has supported a gene-environment interaction between life stress and the serotonin transporter–linked polymorphism (5-HTTLPR) on depression, but few studies have examined factors that influence detection of this effect, despite years of inconsistent results. We propose that the candidate environment (akin to a candidate gene) is key. Theory and evidence have implicated major stressful life events (SLEs)—particularly major interpersonal SLEs—as well as chronic family stress. A total of 400 participants from the Youth Emotion Project (which began with 627 high school juniors oversampled for high neuroticism) completed up to five annual diagnostic and stress interviews and provided DNA samples. A significant gene-environment effect for major SLEs and S-carrier genotype was accounted for significantly by major interpersonal SLEs but not significantly by major noninterpersonal SLEs. S-carrier genotype and chronic family stress also significantly interacted. Identif...

Language development requires both basic cognitive mechanisms for learning language and a rich social context from which learning takes off. Disruptions in learning mechanisms, processing abilities, and/or social interactions increase the risks associated with social exclusion or developmental delays. Given the complexity of language processes, a multilevel approach is proposed where both cognitive mechanisms, genetic and environmental factors need to be probed together with their possible interactions. Here we review and discuss such interplay between environment and genetic predispositions in understanding language disorders, with a particular focus on a possible endophenotype, the ability for statistical sequential learning.

Human language appears to be unique among natural communication systems, and such uniqueness impinges on both nature and nurture. Human babies are endowed with cognitive abilities that predispose them to learn language, and this process cannot operate in an impoverished environment. To be effectively complete the acquisition of human language in human children requires highly socialised forms of learning, scaffolded over years of prolonged and intense caretaker-child interactions. How genes and environment operate in shaping language is unknown. These two components have traditionally been considered as independent, and often pitted against each other in terms of the nature versus nurture debate. This perspective article considers how innate abilities and experience might instead work together. In particular, it envisages potential scenarios for research, in which early caregiver verbal and non-verbal attachment practices may mediate or moderate the expression of human genetic systems for language.

Both expectations towards interactions with conspecifics, and genetic predispositions, affect adults׳ social behaviors. However, the underlying mechanisms remain largely unknown. Here, we report data to investigate the interaction between genetic factors, (oxytocin receptor (OXTR) and serotonin transporter (5-HTTLPR) polymorphisms), and adult interactional patterns in shaping physiological responses to social distress. During the presentation of distress vocalizations (cries of human female, infants and bonobos) we assessed participants׳ (N = 42 males) heart rate (HR) and peripheral nose temperature, which index state of arousal and readiness to action. Self-reported questionnaires were used to evaluate participants' interactional patterns towards peers (Attachment Style Questionnaire, Feeney et al., 1994[1]), and the quality of bond with intimate partners (Experiences in Close Relationships Scale, Fraley et al., 2000 [2]). To assess participants׳ genetic predispositions, the OX...

Language development requires both basic cognitive mechanisms for learning language and a rich social context from which learning takes off. Disruptions in learning mechanisms, processing abilities, and/or social interactions increase the risks associated with social exclusion or developmental delays. Given the complexity of language processes, a multilevel approach is proposed where both cognitive mechanisms, genetic and environmental factors need to be probed together with their possible interactions. Here we review and discuss such interplay between environment and genetic predispositions in understanding language disorders, with a particular focus on a possible endophenotype, the ability for statistical sequential learning.

Human language appears to be unique among natural communication systems, and such uniqueness impinges on both nature and nurture. Human babies are endowed with cognitive abilities that predispose them to learn language, and this process cannot operate in an impoverished environment. To be effectively complete the acquisition of human language in human children requires highly socialised forms of learning, scaffolded over years of prolonged and intense caretaker-child interactions. How genes and environment operate in shaping language is unknown. These two components have traditionally been considered as independent, and often pitted against each other in terms of the nature versus nurture debate. This perspective article considers how innate abilities and experience might instead work together. In particular, it envisages potential scenarios for research, in which early caregiver verbal and non-verbal attachment practices may mediate or moderate the expression of human genetic systems for language.

Background: Scientific enthusiasm about gene 9 environment interactions, spurred by the 5-HTTLPR (serotonin transporter-linked polymorphic region) 9 SLEs (stressful life events) interaction predicting depression, have recently been tempered by sober realizations of small effects and meta-analyses reaching opposing conclusions. These mixed findings highlight the need for further research. Converging evidence suggests that the effects of 5-HTTLPR genotype may be neurodevelopmental in origin, but we are not aware of empirical studies that have investigated whether the 5-HTTLPR genotype 9 SLE interaction predicts preschool-onset depression (PO-MDD), the earliest validated form of depression. Methods: Children (n = 234) aged 3-5 were recruited for a longitudinal study designed to examine PO-MDD. In a comprehensive baseline assessment, the child's primary caregivers completed questionnaires and were interviewed about their child's behaviors, psychiatric symptoms, and exposure to SLEs. Results: A 5-HTTLPR 9 SLEs interaction emerged, such that children homozygous for the short allele were more susceptible to depression in the context of elevated SLE than long allele carriers. In contrast, at low SLE exposure, short allele homozygotes had fewer depressive symptoms. The data were best fit by a plasticity model with a substantial reduction in fit by diathesis-stress models. Conclusions: Extending studies in adult and adolescent populations, these data suggest that 5-HTTLPR genotype may provide plasticity to environmental influence, for better or worse. Specifically, children homozygous for the short allele were more susceptible to the depressogenic effects of SLEs but benefitted, in the form of reduced depressive symptoms, in the context of relatively benign environmental conditions (i.e. relatively low SLE exposure). These data highlight the importance of examining gene 9 environment interactions across development, environment, and outcome but should be interpreted cautiously given the small sample size. 5-HTTLPR, stress, childhood MDD 455 Key points

We conducted a cross-sectional study nested within a cohort study with 276 postpartum women to evaluate the role of a serotonin transporter gene polymorphism (5-HTTLPR) and the stressful life events (SLE) on the risk of postpartum depression (PPD) symptoms in a community sample. Participants were assessed between 45 and 90 days after delivery with the Edinburgh Postnatal Depression Scale (EPDS) and the Mini International Neuropsychiatric Interview (MINI). Data regarding socio-demographic variables, alcohol consumption, tobacco smoking and SLE occurring during pregnancy, were also collected. In the adjusted analysis, the women carrying the long (L) allele (LL) who experienced SLE showed higher prevalence ratios (PR) for PPD symptoms (EPDS !13) than those with two copies of the short (S) allele (SL) (PR ¼ 9.91; 95% confidence interval: 1.70-57.87). In contrast, a trend of association was found between prior history of major depressive disorder (MDD) and the S allele carrier status (p ¼ 0.07). No association was found between the formal diagnosis of current MDD and the 5-HTTLPR genotypes. In line with previous reports, we find in this sample that the L allele carrier status was associated with a heighten risk of depressive symptoms in postpartum when SLE were experienced during pregnancy.

Human observational studies have shown that, in interaction with life stress, the short or S-allele of the serotonin transporter gene-linked polymorphic region (5-HTTLPR) is associated with an enhanced risk for depression. However, this gene-by-environment interaction (G Â E) has recently been questioned by two meta-analyses. We aim to provide an overview and appraisal of recent developments and controversies.

Few studies have investigated the role of gene  environment interactions (G  E) in speech, language, and literacy disorders. Currently, there are two theoretical models, the diathesis-stress model and the bioecological model, that make opposite predictions about the expected direction of G  E, because environmental risk factors may either strengthen or weaken the effect of genes on phenotypes. The purpose of the current study was to test for G  E at two speech sound disorder and reading disability linkage peaks using a sib-pair linkage design and continuous measures of socioeconomic status, home language/literacy environment, and number of ear infections. The interactions were tested using composite speech, language, and preliteracy phenotypes and previously identified linkage peaks on 6p22 and 15q21. Results showed five G  E at both the 6p22 and 15q21 locations across several phenotypes and environmental measures. Four of the five interactions were consistent with the bioecological model of G  E. Each of these four interactions involved environmental measures of the home language/literacy environment. The only interaction that was consistent with the diathesis-stress model was one involving the number of ear infections as the environmental risk variable. The direction of these interactions and possible interpretations are explored in the discussion.

Few studies have investigated the role of gene  environment interactions (G  E) in speech, language, and literacy disorders. Currently, there are two theoretical models, the diathesis-stress model and the bioecological model, that make opposite predictions about the expected direction of G  E, because environmental risk factors may either strengthen or weaken the effect of genes on phenotypes. The purpose of the current study was to test for G  E at two speech sound disorder and reading disability linkage peaks using a sib-pair linkage design and continuous measures of socioeconomic status, home language/literacy environment, and number of ear infections. The interactions were tested using composite speech, language, and preliteracy phenotypes and previously identified linkage peaks on 6p22 and 15q21. Results showed five G  E at both the 6p22 and 15q21 locations across several phenotypes and environmental measures. Four of the five interactions were consistent with the bioecological model of G  E. Each of these four interactions involved environmental measures of the home language/literacy environment. The only interaction that was consistent with the diathesis-stress model was one involving the number of ear infections as the environmental risk variable. The direction of these interactions and possible interpretations are explored in the discussion.

Few studies have investigated the role of gene  environment interactions (G  E) in speech, language, and literacy disorders. Currently, there are two theoretical models, the diathesis-stress model and the bioecological model, that make opposite predictions about the expected direction of G  E, because environmental risk factors may either strengthen or weaken the effect of genes on phenotypes. The purpose of the current study was to test for G  E at two speech sound disorder and reading disability linkage peaks using a sib-pair linkage design and continuous measures of socioeconomic status, home language/literacy environment, and number of ear infections. The interactions were tested using composite speech, language, and preliteracy phenotypes and previously identified linkage peaks on 6p22 and 15q21. Results showed five G  E at both the 6p22 and 15q21 locations across several phenotypes and environmental measures. Four of the five interactions were consistent with the bioecological model of G  E. Each of these four interactions involved environmental measures of the home language/literacy environment. The only interaction that was consistent with the diathesis-stress model was one involving the number of ear infections as the environmental risk variable. The direction of these interactions and possible interpretations are explored in the discussion.

Few studies have investigated the role of gene  environment interactions (G  E) in speech, language, and literacy disorders. Currently, there are two theoretical models, the diathesis-stress model and the bioecological model, that make opposite predictions about the expected direction of G  E, because environmental risk factors may either strengthen or weaken the effect of genes on phenotypes. The purpose of the current study was to test for G  E at two speech sound disorder and reading disability linkage peaks using a sib-pair linkage design and continuous measures of socioeconomic status, home language/literacy environment, and number of ear infections. The interactions were tested using composite speech, language, and preliteracy phenotypes and previously identified linkage peaks on 6p22 and 15q21. Results showed five G  E at both the 6p22 and 15q21 locations across several phenotypes and environmental measures. Four of the five interactions were consistent with the bioecological model of G  E. Each of these four interactions involved environmental measures of the home language/literacy environment. The only interaction that was consistent with the diathesis-stress model was one involving the number of ear infections as the environmental risk variable. The direction of these interactions and possible interpretations are explored in the discussion.

Few studies have investigated the role of gene  environment interactions (G  E) in speech, language, and literacy disorders. Currently, there are two theoretical models, the diathesis-stress model and the bioecological model, that make opposite predictions about the expected direction of G  E, because environmental risk factors may either strengthen or weaken the effect of genes on phenotypes. The purpose of the current study was to test for G  E at two speech sound disorder and reading disability linkage peaks using a sib-pair linkage design and continuous measures of socioeconomic status, home language/literacy environment, and number of ear infections. The interactions were tested using composite speech, language, and preliteracy phenotypes and previously identified linkage peaks on 6p22 and 15q21. Results showed five G  E at both the 6p22 and 15q21 locations across several phenotypes and environmental measures. Four of the five interactions were consistent with the bioecological model of G  E. Each of these four interactions involved environmental measures of the home language/literacy environment. The only interaction that was consistent with the diathesis-stress model was one involving the number of ear infections as the environmental risk variable. The direction of these interactions and possible interpretations are explored in the discussion.

Few studies have investigated the role of gene  environment interactions (G  E) in speech, language, and literacy disorders. Currently, there are two theoretical models, the diathesis-stress model and the bioecological model, that make opposite predictions about the expected direction of G  E, because environmental risk factors may either strengthen or weaken the effect of genes on phenotypes. The purpose of the current study was to test for G  E at two speech sound disorder and reading disability linkage peaks using a sib-pair linkage design and continuous measures of socioeconomic status, home language/literacy environment, and number of ear infections. The interactions were tested using composite speech, language, and preliteracy phenotypes and previously identified linkage peaks on 6p22 and 15q21. Results showed five G  E at both the 6p22 and 15q21 locations across several phenotypes and environmental measures. Four of the five interactions were consistent with the bioecological model of G  E. Each of these four interactions involved environmental measures of the home language/literacy environment. The only interaction that was consistent with the diathesis-stress model was one involving the number of ear infections as the environmental risk variable. The direction of these interactions and possible interpretations are explored in the discussion.

Response to antidepressants is interindividually variable. It has been suggested that this variability is a direct consequence of etiological heterogeneity. Therefore, the same genes, environments, and gene–environment interactions implicated in different etiological pathways to depression may also predict response to treatment. This article reviews the evidence relevant to this hypothesis by first outlining the roles of genes, environments, and gene–environment interplay in the etiology of depression, and then considering the same factors in treatment response. Environmental exposures, such as childhood maltreatment, are potent predictors of both depression and treatment response. Although alone genetic factors have failed to consistently predict either phenotype, several polymorphisms have been shown to moderate the effects of environmental adversity on the development of depression and treatment response. These findings suggest that the dissection of etiological pathways to depression may provide the key to understanding and predicting response to antidepressants.