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Results for “gene-environment correlations”

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PubMed2026

Methods for modeling gene-environment interplay using polygenic risk scores.

Polygenic risk scores (PRS) are increasingly recognized as pivotal tools for quantifying disease risk through the aggregation of multiple genetic variants. As sample sizes in genome-wide association studies (GWAS) continue to expand and PRS become more powerful, they are set to play a key role in translational research and personalized medicine. Understanding the interplay of PRS with environmental factors is critical for interpreting and applying PRS in diverse contexts. This interplay manifests in two forms: PRS-by-environment interaction (PRS × E) and gene-environment correlation (rGE). However, despite the growing application and importance of PRS, there are limited guidelines for performing PRS × E interaction analyses while controlling for rGE, which can lead to inconsistencies across studies and misinterpretation of results. Here we provide a review of different methods for performing PRSxE interaction in various epidemiological study designs, propose recommendations for best-practice, and discuss future challenges.

Gene-Environment Interaction↗

PubMed2026

Genetic risk scores, perceived neighborhood disorder, and sleep duration.

STUDY OBJECTIVES: Most studies of neighborhood context and sleep health emphasize direct effects and fail to account for the role of genetics. In this paper, we draw on the socioecological model to examine the interplay of genetics, neighborhood context, and sleep health. We specifically examine the independent and joint effects of genetic risk scores (GRS) and perceived neighborhood disorder on sleep duration. METHODS: We combine genomic and cross-sectional survey data from the All of Us Research Program, a non-probability sample of 22 575 adults of European ancestry living in the United States. We use the sleep duration-increasing risk allele count for 78 genome-wide single nucleotide polymorphisms (SNPs) to construct weighted genetic risk scores. Our analyses include an index of perceived neighborhood disorder and an objective measure of sleep duration based on wrist actigraphy. RESULTS: Genetic risk scores are inversely associated with neighborhood disorder, positively associated with continuous sleep duration, and inversely associated with the odds of short sleep. Neighborhood disorder is inversely associated with continuous sleep duration and positively associated with the odds of short and long sleep. The association between genetic risk scores and sleep duration (continuous and categorical) is invariant across levels of neighborhood disorder. CONCLUSIONS: Our analyses confirm the independent direct effects of genetic risk scores and neighborhood disorder on sleep duration. Our findings extend the socioecological model by assessing the role of genetics in the study of neighborhood context and sleep health. Although we observed a gene-environment correlation between genetic risk scores and perceived neighborhood disorder, there was little indication of genetic confounding and no evidence of gene-environment interaction.

Humans↗

PubMed1992

Fitting genetic models to Carabelli trait data in South Australian twins.

This study aimed to clarify genetic and environmental contributions to Carabelli trait variation on permanent first molar teeth in a large sample of South Australian twins. Estimates of polychoric correlations were obtained between pairs of monozygous (MZ) and dizygous (DZ) twins for Carabelli data and various gene-environment models fitted by a weighted least-squares approach. The favored model included additive genetic effects together with both a general environmental component and an environmental effect specific to each side. An estimate of heritability around 90% indicated a very strong genetic contribution to observed variation. The pattern of correlations for MZ and DZ data suggested that further studies involving other types of relatives would be worthwhile for detection of possible non-additive genetic effects of dominance or epistasis.

Adolescent↗

PubMed1987

Twin study on myopia.

In order to reassess the relative importance of genetic and environmental factors in the development of myopia in Chinese schoolchildren, 90 pairs of MZ and 36 pairs of like-sex DZ twins were enrolled for detailed ophthalmological examination about their ocular refractions. Corneal curvatures and axial lengths were also measured. With equivalent settings of the range for concordance, corneal curvatures showed higher concordance rate (84%) than ocular refractions (65%) and axial lengths (59%) in MZ twins. F-test on the intrapair variances between MZ and DZ twins revealed a significant hereditary role in determining the ocular refraction and its optical components. The degree of genetic determination was expressed by heritability indices, which were derived from intraclass correlation coefficients. The diversity of sample ages and refractions, while making the obtained data difficult to further explore the gene-environment interaction, led to the observation of more intrapair differences with age and myopic progression in MZ twins.

Adolescent↗

PubMed1992

Genetic and environmental determinants of factor VII coagulant activity in ethnic groups at differing risk of coronary heart disease.

It has been shown previously that individuals possessing the Gln353 allele of factor VII have significantly lower factor VIIc levels. In this population based study of Europeans, Afro-Caribbeans and Gujarati Indians, the Gln353 allele was associated with lower factor VIIc in all groups, carriers having factor VIIc levels 20-25% below the group mean. Although the Afro-Caribbeans had the lowest factor VIIc levels, the frequency of the Gln353 allele was not different from the European sample. However, in the Gujaratis, the frequency of the Gln353 allele was significantly higher than in the Europeans (0.25 compared to 0.09, P less than 0.001). Factor VIIc is known to be positively correlated with plasma triglyceride levels, although the Gujaratis, having the highest mean triglyceride levels, did not have the highest mean factor VIIc levels. On examination of the relationship between triglycerides and factor VIIc in the Gujaratis there was a correlation (r = 0.23, P = 0.13) in individuals homozygous for the factor VII Arg353 allele, but no correlation (r = 0.001, P = 0.5) among Gln353 carriers. This striking difference suggests that the effect of triglycerides on factor VIIc is genotype specific and thus provides an example of gene-environment interaction. The high frequency of the Gln353 allele, with its associated lack of relationship between triglyceride and factor VIIc levels, may explain the lower than expected factor VIIc levels in the Gujaratis.

Africa↗

PubMed1985

Selection for life span in Drosophila melanogaster.

Selection for reproduction at an early or a late age in life was applied to populations of D. melanogaster for 21 to 29 generations, with two experimental treatments of larval density. Populations with high and uncontrolled numbers of competing larvae responded strongly to selection for late-reproduction with the length of adult life increasing by as much as 50 per cent. In this treatment, selection produced true breeding long- and short-lived lines. When populations of developing larvae were held low, however, longevity fluctuated wildly during selection, showing little overall response, as several previous tests of senescence theory have also found. These experiments suggest that life span is either physiologically limited in that environment, or populations are unable to respond because either phenotype/genotype correlations are reversed, or genetic variation is suppressed. The inability of former studies to obtain a response to selection appears to have resulted from the artifactual introduction of strong gene-environment interactions through the use of a competition-free environment.

Animals↗

PubMed1987

Transmission of human craniofacial dimensions.

The transmissibilities of 11 human craniofacial dimensions are estimated by path analysis based upon familial correlations obtained in four different populations. Estimates from both the individual populations and from pooled correlations indicate that the observed variation in craniofacial dimensions is determined by genetic and nongenetic factors in roughly equal measure (.45 less than t 2 less than .60). These results implicate the possibility of complex gene-environment and gene-gene interactions in the development of the size and shape of the head and face and call for more detailed familial studies of these traits. This additional complexity further suggests the need for caution in interpreting such metrical variation, especially from a diagnostic or classificatory viewpoint.

Canada↗

PubMed2026

Variance Polygenic Scores (vPGS) as a Tool for Studying Gene-Environment Interactions Associated With Refractive Error.

PURPOSE: Conventional polygenic scores predict an individual's phenotype based on their genetics. By contrast, variance polygenic scores (vPGS) quantify genetic predisposition to phenotypic variance. We tested the hypothesis that a vPGS for refractive error can identify individuals with increased susceptibility to environmental risk factors for myopia. METHODS: Six vPGS construction strategies were evaluated in UK Biobank participants: three variance heterogeneity genome-wide association study (vGWAS) methods and two reweighting schemes. vPGS performance was assessed using two metrics: (i) "Diff"-difference in phenotypic variance in vPGS decile ten versus one; (ii) Spearman correlation of phenotypic variance versus vPGS decile. The optimal vPGS was used to test for vPGS × time spent reading or vPGS × time spent outdoors interactions in children aged 15 years (ALSPAC cohort; n = 3471). RESULTS: Of the vGWAS methods, conditional quantile regression outperformed SCAMPI and Levene's Test. Of the re-weighting schemes, LDpred2 outperformed pruning and thresholding. In an independent sample of UK Biobank participants (n = 19,470), the top-performing vPGS successfully stratified individuals into groups with increasing variance in refractive error, even after adjusting for a conventional PGS (Diff: 2.55, 95% confidence interval [CI], 1.64-3.47; Spearman correlation = 0.87; 95% CI, 0.43-0.93). However, in ALSPAC participants, there was minimal support for vPGS interactions with time reading (P = 0.80) or time outdoors (P = 0.89). CONCLUSIONS: A novel vPGS successfully stratified individuals into groups with relatively high or low genetic susceptibility to refractive error variance. However, the vPGS could not identify individuals at enhanced risk from lifestyle risk factors for myopia.

Humans↗

PubMed1992

Numerical comparisons of two formulations of the logistic regressive models with the mixed model in segregation analysis of discrete traits.

Segregation analysis of discrete traits can be conducted by the classical mixed model and the recently introduced regressive models. The mixed model assumes an underlying liability to the disease, to which a major gene, a multifactorial component, and random environment contribute independently. Affected persons have a liability exceeding a threshold. The regressive logistic models assume that the logarithm of the odds of being affected is a linear function of major genotype effects, the phenotypes of older relatives, and other covariates. A formulation of the regressive models, based on an underlying liability model, has been recently proposed. The regression coefficients on antecedents are expressed in terms of the relevant familial correlations and a one-to-one correspondence with the parameters of the mixed model can thus be established. Computer simulations are conducted to evaluate the fit of the two formulations of the regressive models to the mixed model on nuclear families. The two forms of the class D regressive model provide a good fit to a generated mixed model, in terms of both hypothesis testing and parameter estimation. The simpler class A regressive model, which assumes that the outcomes of children depend solely on the outcomes of parents, is not robust against a sib-sib correlation exceeding that specified by the model, emphasizing testing class A against class D. The studies reported here show that if the true state of nature is that described by the mixed model, then a regressive model will do just as well. Moreover, the regressive models, allowing for more patterns of family dependence, provide a flexible framework to understand gene-environment interactions in complex diseases.

Computer Simulation↗

PubMed1991

Regressive logistic models for familial diseases: a formulation assuming an underlying liability model.

Statistical models have been developed to delineate the major-gene and non-major-gene factors accounting for the familial aggregation of complex diseases. The mixed model assumes an underlying liability to the disease, to which a major gene, a multifactorial component, and random environment contribute independently. Affection is defined by a threshold on the liability scale. The regressive logistic models assume that the logarithm of the odds of being affected is a linear function of major genotype, phenotypes of antecedents and other covariates. An equivalence between these two approaches cannot be derived analytically. I propose a formulation of the regressive logistic models on the supposition of an underlying liability model of disease. Relatives are assumed to have correlated liabilities to the disease; affected persons have liabilities exceeding an estimable threshold. Under the assumption that the correlation structure of the relatives' liabilities follows a regressive model, the regression coefficients on antecedents are expressed in terms of the relevant familial correlations. A parsimonious parameterization is a consequence of the assumed liability model, and a one-to-one correspondence with the parameters of the mixed model can be established. The logits, derived under the class A regressive model and under the class D regressive model, can be extended to include a large variety of patterns of family dependence, as well as gene-environment interactions.

Environment↗

PubMed2026

Novel epigenetic loci identified from an epigenome-wide association study underlying brain structural changes in bipolar disorder.

BACKGROUND: DNA methylation influences gene-environment interactions and brain development in bipolar disorder (BD). We aimed to identify BD-associated epigenetic loci and examine their associations with brain structural variation. METHODS: We conducted an epigenome-wide association study (BD group, n = 90; healthy controls group, n = 161) to identify BD-associated DNA methylation loci, and we additionally performed copy number alteration and functional enrichment analyses. The correlations between epigenetic loci and cortical thickness (CT) were assessed using Pearson's partial correlation analysis, and the co-methylation effect of the epigenetic loci identified in the neuroimaging-epigenetic analysis was investigated. FINDINGS: A total of 156 differentially methylated positions (DMPs) and 7 differentially methylated regions were identified, and the genes associated with them were observed to be enriched in biological processes related to muscle hypertrophy and neuronal activity. Significant correlations between the methylation levels of 13 DMPs associated with three genes (miR886, PLEC1, and ICAM5) and the CT of the right postcentral gyrus and inferior frontal gyrus were identified. Specifically, 10 DMPs associated with the CpG island in the upstream region of the miR886 gene showed negative correlations with the right postcentral gyrus CT, implicating miR886-associated CpG-island methylation in regional cortical thinning. CONCLUSION: Epigenetic changes might play an important role in brain structural changes in BD. These multimodal findings nominate miR886-related methylation as a candidate molecular correlate of cortical thinning and warrant replication and mechanistic follow-up in larger, state-diverse cohorts.

Humans↗

PubMed1990

Study of gene-environment effects on development of hyperopia: a study of 191 adult twin pairs from the Finnish Twin Cohort Study.

The Finnish Twin Cohort material was used to estimate genetic and environmental effects in the etiology of hyperopia (farsightedness). All twin pairs in the cohort born before year 1927 (age 60 years and over at the time of the study), with both members alive, were sent a questionnaire. The questionnaire included questions of past and present eye diseases, visits to ophthalmologists, use of glasses and other vision-related questions. The hyperopia was assessed by asking the patients to send their last prescription for glasses to the authors. Twins with any eye disease affecting refraction (cataract, corneal damage), operation or trauma to their eyes were discarded from the present study. In 191 pairs (80 monozygotic and 111 dizygotic pairs) one or both members of the pair had a hyperopic refractive error. The correlations of refraction between right and left eyes of both MZ and DZ pairs were high (Spearman Rank Correlations of 0.86-0.89). The intrapair correlations among MZ pairs were higher (0.44 for right and 0.45 for left eyes) than intrapair correlations among DZ pairs (0.24 for right and 0.15 for left eyes). The variances were not significantly different among MZ and DZ pairs. The classical analysis of heritability gave an estimate of 0.75 for hyperopia. The result suggests that genetic factors are important in hyperopia and especially in hyperopia of higher degree.

Adult↗

PubMed2026

Using high-dimensional environmental covariates to study genotype by environment interaction for reproductive traits in Duroc boars.

We investigated the potential of incorporating grid-cell-based environmental covariates (ECs) in the genetic evaluation of total sperm count (TSC), sperm motility (MOT), and sperm morphology (MOR) for Duroc boars. A total of 188,665 records derived from 3,684 genotyped boars, born between December 2018 and October 2024 and raised in three stud farms located in different U.S. states, were analyzed using multi-trait linear-threshold repeatability models. To account for genotype by environment interactions (GE), we constructed an interaction matrix as the Hadamard product of the genomic relationship matrix and an environmental (co)variance matrix. The environmental groups were defined in three ways: farm, farm-season, and farm-year-season. The (co)variance matrix was constructed based on daily ECs obtained from the NASA POWER database for each environmental group. Of all available ECs, those significantly associated with TSC, MOT, and MOR (temperature, relative humidity, atmospheric pressure, and wind speed and direction) were retained. We evaluated five models with different GE structures: M1 represented the baseline without accounting for GE, in M2 the GE included farm as environmental groups, in M3 the GE included farm-season as environmental groups, in M4 the GE included farm-year-season as environmental groups, and M5 involved M3 with an additional random effect of the farm-season. Estimates of heritability for TSC, MOT, and MOR ranged from 0.03 to 0.04, 0.05 to 0.08, and 0.04 to 0.08, respectively. Corresponding repeatability ranged from 0.15 to 0.23, 0.28 to 0.49, and 0.28 to 0.49. The proportion of phenotypic variance attributed to GE variance ranged from 0.00 to 0.32, 0.00 to 0.44, and 0.00 to 0.44. Lastly, estimates of genetic correlation, TSC-MOT, TSC-MOR, and MOT-MOR ranged from 0.27 to 0.31, 0.24 to 0.31, and 0.98 to 0.99, respectively, with minor differences across models. We assessed the predictive ability of models using the linear regression validation. Across traits and models, bias ranged from -0.05 to 0.02 standard deviations, slope varied from 0.88 to 0.99, the correlation ranged from 0.75 to 0.84, and accuracy from 0.41 to 0.53. Overall, building the GE matrix considering grid-cell-based ECs helped to account for GE, thereby reducing the proportion of phenotypic variance attributed to genetic components; however, it did not improve the validation metrics. Additional on-farm records for ECs may improve the model performance.

Animals↗

PubMed1992

Gene-environment interaction in hypertension, stroke and atherosclerosis in experimental models and supportive findings from a world-wide cross-sectional epidemiological survey: a WHO-cardiac study.

1. Genetic rat models of hypertension, such as spontaneously hypertensive rats (SHR) and in particular, stroke-prone SHR (SHRSP) are useful models for research on the genetic pathogenesis, gene-environment interaction and control of environmental factors for the prevention of hypertension and related cardiovascular diseases (CVD). 2. Since recent genetic analysis of hypertension in SHRSP indicated that one of the hypertensive genes related to salt-induced blood pressure (BP) rise was linked with the gene of the angiotensin-converting enzyme, gene-environment interaction is important in the humoral, neural, vascular and nutritional mechanisms of hypertension and CVD. 3. Extensive experimental studies in SHRSP by the authors have demonstrated nutritional factors counteracting directly or indirectly against the adverse effect of excess salt intake, such as K, Mg, Ca, dietary fibres, protein, some amino acids and fatty acids, etc.; they are therefore effective in preventing stroke, the typical complication of hypertension. 4. Experimental atherosclerotic models were established in SHRSP, which indicated also a gene-environment interaction in the pathogenesis of atherosclerosis at the cellular level of vascular smooth muscle cells. Excess salt intake accelerated cholesterol absorption from the intestine to induce arterial fat deposition as well as to active platelet aggregation by the mechanism of increased intracellular Ca2+ mobilization. 5. Based on such experimental findings on the hypertension and related CVD prevention, a cross-sectional multicentre epidemiological 'CVD and Alimentary Comparison' Study (WHO-CARDIAC Study) was designed to assess the relationship of biological markers of dietary factors with BP ('core' study) and major CVD mortalities ('complete' study) and has been successfully undertaken for the past 8 years in co-operation with 54 centres in 23 countries. 6. The results of 'core' study so far obtained by cross-centre simple linear regression analysis demonstrated adverse effects of body mass index and salt intake on BP in men and possible beneficial effects of Mg by within-centre multiple linear regression analysis. 7. Preliminary cross-centre simple linear regression analysis of the 'complete' study indicated a positive correlation of serum cholesterol levels and negative correlation of serum phospholipid poly-unsaturated to unsaturated fatty acid ratios and 24 h urinary taurine excretion with coronary heart diseases mortality; a positive correlation of 24 h urinary Na and Na/K ratios and a negative correlation of serum cholesterol levels with stroke mortalities was indicated. 8. These epidemiological data confirmed mostly the applicability of experimental findings to the nutritional prevention of hypertension and CVD prevention.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed2026

Humanizing acidic mammalian chitinase variants establish lung immune conditioning and control environmentally driven inflammation and fibrosis.

Chitin, a widespread environmental particle constituent, triggers lung inflammation but is degraded by chitinases. In humans, single-nucleotide polymorphisms (SNPs) in CHIA (acidic mammalian chitinase; AMCase) are associated with lung disease, suggesting that chitinase variants influence responses to airborne particles. Here, we edit the mouse Chia1 locus to generate humanized (hChia) mice harboring common human SNPs. Compared with controls expressing disease-protective SNPs, hChia mice lack robust chitinase activity and fail to degrade natural chitin substrates. Lung-resident lymphocytes and macrophages are spontaneously primed and sensitive to inflammatory triggering by environmental chitin. Immune cell infiltration correlates with airway chitin following challenge, and hChia mice exhibit exacerbated inflammatory and fibrotic lung disease. In humans with acute respiratory failure, alveolar hemorrhage coincides with environmentally derived chitin particles that are susceptible to chitinase degradation, attenuating inflammatory cell responses. Thus, environmental chitin and chitinase activity are crucial determinants of lung immune conditioning with potential therapeutic applications.

AMCase↗

PubMed2025

Identification of a novel heterozygous GPD1 missense variant in a Chinese adult patient with recurrent HTG-AP consuming a high-fat diet and heavy smoking.

BACKGROUND: Glycerol-3-phosphate dehydrogenase 1 (GPD1) gene defect can cause hypertriglyceridemia (HTG), which usually occurs in infants. The gene defect has rarely been reported in adult HTG patients. In the present study, we described the clinical and functional analyses of a novel GPD1 missense variant in a Chinese adult patient with recurrent hypertriglyceridemia‑related acute pancreatitis (HTG-AP), consuming a high-fat diet and smoking heavily. METHODS: Exome sequencing was used to analyze the DNA of the adult patient's blood sample. It was found that there was a new variant of GPD1 gene-p.K327N, which was verified by gold standard-sanger sequencing method. In vitro, the corresponding plasmid was constructed and transfected into human renal HEK-293T cells, and GPD1 protein levels were detected. A biogenic analysis was performed to study the population frequency, conservation, and electric potential diagram of the new variant p.K327N. Finally, the previously reported GPD1 variants were sorted and their phenotypic relationships were compared. RESULTS: A novel heterozygous variant of GPD1, p.K327N (c.981G > C), was found in the proband. Furthermore, the patient's daughter carried this variant, whereas his wife did not carry the variant. The proband with obesity suffered eight episodes of HTG-AP from the age of 36 years, and each onset of AP was correlated to high-fat diet consumption and heavy smoking. In vitro, this variant exerted a relatively mild effect on GPD1 functions, which were associated with its effect upon secretion (~ 25% of secretion decreased compared with that of the wild-type); thus, eventually impairing protein synthesis. Additionally, 36 patients with GPD1 variants found in previous studies showed significant transient HTG in infancy. The proband carrying the GDP1 variant was the first reported adult with recurrent HTG-AP. CONCLUSION: We identified a novel GPD1 variant, p.K327N, in a Chinese adult male patient with recurrent HTG-AP. The variant probably exerted a mild effect on GPD1 functions. The heterozygosity of this GPD1 variant, in addition to high-fat diet consumption and heavy smoking, probably triggered HTG-AP in the patient.

Adult↗

PubMed1990

Bivariate survival models for analysis of genetic and environmental effects in twins.

Classic methods in genetics for the analysis of binary attributes, based on an assumption of a "threshold" on a normally distributed latent variable called "liability," estimate the strength of genetic and environmental effects from differences in correlations between relatives of differing genetic relatedness. Two problems that are not easily addressed by these methods are the need to take the age of onset into account (particularly in chronic diseases in which incidence rates vary considerably with age and the lengths of time at risk can vary between individuals) and the desirability of incorporating measured covariates (genetic or environmental). The standard methods of cohort analysis used in epidemiology allow for both of these features, but until recently have been restricted to independent individuals. Recent developments in survival analysis have extended the widely used "proportional hazards" model of Cox by the addition of latent variable, epsilon, reflecting the shared susceptibility of related subjects because of their shared genes or shared environment. We show how this approach can be combined with more traditional models of gene-environment interaction to allow the main effects of measured genetic markers and environmental variables to be estimated, as well as the residual variance of genetic and environment and their interactions. The approaches are applied to a cohort of female twin births in Sweden from 1886 to 1958, linked with the Swedish cancer registry from 1961 to 1982.

Adult↗

PubMed2025

Haplotype stacking to improve stability of stripe rust resistance in wheat.

Genotype-by-environment interaction analysis and haplotype-level characterisation provide novel insights into the stability of stripe rust resistance. Breeding selection strategies are proposed to achieve rapid and stable genetic gains across environments. This study investigated stripe/yellow rust (YR) responses in the Vavilov wheat diversity panel evaluated across 11 field experiments conducted in Australia and Ethiopia during 2014-2021. Genotype-by-environment interaction (GEI) was analysed using a factor analytic (FA) model. Genotype-level selection was performed with overall performance (OP) and root-mean-square deviation (RMSD), which reflected average performance and stability of YR resistance across environments, respectively. Genomic estimated breeding values (GEBV) for these traits were calculated and compared with those from a multi-trait GBLUP model with average performance represented by the mean GEBV across environments and stability by the standard deviation of GEBV across environments. The FA-based and multi-trait GBLUP GEBV had high correlations. Haplotypes with large effects on OP and RMSD were identified using the local GEBV method. Favourable haplotypes were then used for stacking in breeding simulations, using the Vavilov collection as a base. Compared to truncation selection, optimal haplotype selection (OHS) using an artificial intelligence (AI)-based algorithm achieved longer-term genetic gains for both OP and RMSD (after many generations) by initially selecting founder parents that maximised favourable haplotypes. Simulations using YR responses from diverse environments that mimicked fluctuating environmental conditions across seasons were conducted to evaluate strategies for selection of YR resistance that is stable across years. Strategies which gave most weight to OP, but some weight to RMSD were optimal in these conditions, and substantially reduced variation of performance across years. This study provides useful information for breeding cultivars with both high YR resistance and high stability of resistance across environments.

Triticum↗