Evidence For Genetic Correlation Research Articles

The ecology and quantitative genetics of seed and seedling traits in upland and lowland ecotypes of a perennial grass.

Plants have evolved diverse reproductive allocation strategies and seed traits to aid in dispersal, persistence in the seed bank, and establishment. In particular, seed size, dormancy, and early seedling vigor are thought to be key functional traits with important recruitment and fitness consequences across abiotic stress gradients. Selection for favored seed-trait combinations, or against maladaptive combinations, is likely an important driver shaping recruitment strategies. Here, we test for seed-trait plasticity and patterns of recruitment using two genotypes representative of contrasting upland and lowland ecotypes of Panicum hallii with field experiments in native versus foreign habitats. Furthermore, we test whether seed traits have been under directional selection in P. hallii using the v-test based on trait variance in a genetic cross. Finally, we evaluate the genetic architecture of ecotypic divergence for these traits with quantitative trait locus (QTL) mapping. Field experiments reveal little plasticity but support a hypothesis of adaptation divergence among ecotypes based on recruitment. Patterns of segregation within recombinant hybrids provides strong support for directional selection driving ecotypic divergence in seed traits. Genetic mapping revealed a polygenic architecture with evidence of genetic correlation between seed mass, dormancy, and seedling vigor. Our results suggest that the evolution of these traits may involve constraints that affect the direction of adaptive divergence. For example, seed size and germination percentage shared two colocalized QTL with antagonistic additive effects. This supports the hypothesis of a functional genetic relationship between these traits, resulting in either large seed/strong dormancy or small seed/weak dormancy trait combinations. Overall, our study provides insights into the factors facilitating and potentially constraining ecotypic differentiation in seed traits.

The relationships between women\u2019s reproductive factors: a Mendelian randomisation analysis

BackgroundWomen’s reproductive factors include their age at menarche and menopause, the age at which they start and stop having children and the number of children they have. Studies that have linked these factors with disease risk have largely investigated individual reproductive factors and have not considered the genetic correlation and total interplay that may occur between them. This study aimed to investigate the nature of the relationships between eight female reproductive factors.MethodsWe used data from the UK Biobank and genetic consortia with data available for the following reproductive factors: age at menarche, age at menopause, age at first birth, age at last birth, number of births, being parous, age first had sexual intercourse and lifetime number of sexual partners. Linkage disequilibrium score regression (LDSC) was performed to investigate the genetic correlation between reproductive factors. We then applied Mendelian randomisation (MR) methods to estimate the causal relationships between these factors. Sensitivity analyses were used to investigate directionality of the effects, test for evidence of pleiotropy and account for sample overlap.ResultsLDSC indicated that most reproductive factors are genetically correlated (rg range: |0.06–0.94|), though there was little evidence for genetic correlations between lifetime number of sexual partners and age at last birth, number of births and ever being parous (rg < 0.01). MR revealed potential causal relationships between many reproductive factors, including later age at menarche (1 SD increase) leading to a later age at first sexual intercourse (beta (B) = 0.09 SD, 95% confidence intervals (CI) = 0.06,0.11), age at first birth (B = 0.07 SD, CI = 0.04,0.10), age at last birth (B = 0.06 SD, CI = 0.04,0.09) and age at menopause (B = 0.06 SD, CI = 0.03,0.10). Later age at first birth was found to lead to a later age at menopause (B = 0.21 SD, CI = 0.13,0.29), age at last birth (B = 0.72 SD, CI = 0.67, 0.77) and a lower number of births (B = −0.38 SD, CI = −0.44, −0.32).ConclusionThis study presents evidence that women’s reproductive factors are genetically correlated and causally related. Future studies examining the health sequelae of reproductive factors should consider a woman’s entire reproductive history, including the causal interplay between reproductive factors.

Leveraging Genetic Data to Elucidate the Relationship Between COVID-19 and Ischemic Stroke.

BackgroundThe relationship between COVID‐19 and ischemic stroke is poorly understood due to potential unmeasured confounding and reverse causation. We aimed to leverage genetic data to triangulate reported associations.Methods and ResultsAnalyses primarily focused on critical COVID‐19, defined as hospitalization with COVID‐19 requiring respiratory support or resulting in death. Cross‐trait linkage disequilibrium score regression was used to estimate genetic correlations of critical COVID‐19 with ischemic stroke, other related cardiovascular outcomes, and risk factors common to both COVID‐19 and cardiovascular disease (body mass index, smoking and chronic inflammation, estimated using C‐reactive protein). Mendelian randomization analysis was performed to investigate whether liability to critical COVID‐19 was associated with increased risk of any cardiovascular outcome for which genetic correlation was identified. There was evidence of genetic correlation between critical COVID‐19 and ischemic stroke (rg=0.29, false discovery rate [FDR]=0.012), body mass index (rg=0.21, FDR=0.00002), and C‐reactive protein (rg=0.20, FDR=0.00035), but no other trait investigated. In Mendelian randomization, liability to critical COVID‐19 was associated with increased risk of ischemic stroke (odds ratio [OR] per logOR increase in genetically predicted critical COVID‐19 liability 1.03, 95% CI 1.00–1.06, P‐value=0.03). Similar estimates were obtained for ischemic stroke subtypes. Consistent estimates were also obtained when performing statistical sensitivity analyses more robust to the inclusion of pleiotropic variants, including multivariable Mendelian randomization analyses adjusting for potential genetic confounding through body mass index, smoking, and chronic inflammation. There was no evidence to suggest that genetic liability to ischemic stroke increased the risk of critical COVID‐19.ConclusionsThese data support that liability to critical COVID‐19 is associated with an increased risk of ischemic stroke. The host response predisposing to severe COVID‐19 is likely to increase the risk of ischemic stroke, independent of other potentially mitigating risk factors.

Joint Analysis of Genome-Wide Association Data Reveals No Genetic Correlations Between Low Back Pain and Neurodegenerative Diseases.

Background: We aimed to explore the genetic correlation and bidirectional causal relationships between low back pain (LBP) and three neurodegenerative diseases, Alzheimer’s disease (AD), Parkinson’s disease (PD), and amyotrophic lateral sclerosis (ALS).Methods: Summary-level statistics were obtained from genome-wide association studies of LBP (n = 177,860), AD (n = 63,926), PD (n = 482,730), and ALS (n = 80,610). We implemented linkage disequilibrium score regression to calculate heritability estimates and genetic correlations. To investigate possible causal associations between LBP and three neurodegenerative diseases, we also conducted a bidirectional two-sample Mendelian randomization (MR) study. Inverse variance-weighted MR was employed as the primary method to generate overall estimates, whereas complementary approaches and sensitivity analyses were conducted to confirm the consistency and robustness of the findings.Results: There was no evidence of genetic correlations between LBP and AD (Rg = −0.033, p = 0.766). MR analyses did not support the causal effect of LBP on AD (OR = 1.031; 95% CI, 0.924–1.150; p = 0.590) or the effect of AD on LBP (OR = 0.963; 95% CI, 0.923–1.006; p = 0.090). Likewise, this study failed to identify genetic correlations between LBP and two other neurodegenerative diseases. MR results of the associations of LBP with PD and ALS, and the reverse associations, did not reach Bonferroni-corrected significance.Conclusion: The study did not support genetic correlations or causations between LBP and three common neurodegenerative diseases, AD, PD, and ALS in the European population.

Assessing the genetic relationships between osteoarthritis and human plasma proteins: a large scale genetic correlation scan.

BackgroundOsteoarthritis (OA) is a multifactorial complex disease. The impact of plasma proteins on OA remains elusive now.MethodsThe UK Biobank genome-wide association study data of OA was used here. Genome-wide SNP genotyping was performed using the Affymetrix UK BiLEVE Axiom or UK Biobank Axiom array. Equally, the GWAS summary data of 3,622 plasma proteins was derived from a recently published study. Consequently, linkage disequilibrium score regression (LD score regression) analysis was performed to evaluate the genetic correlation between each plasma protein and different sites of OA.ResultsSeveral suggestive plasma proteins were identified for OA. For hand OA, evidence of genetic correlation was observed for inter-alpha-trypsin inhibitor heavy chain H1 (coefficient =−0.3854, P value =0.0198), multiple inositol polyphosphate phosphatase 1 (coefficient =−1.1721, P value =0.0303). For hip OA, 7 suggestive genetic correlation signals were observed, such as Transmembrane glycoprotein NMB (coefficient =0.6944, P value =0.0098), Endothelial cell-specific molecule 1 (coefficient =0.6337, P value =0.03). For Knee OA, 12 suggestive genetic correlation signals were identified, including Elafin (coefficient =−0.5562, P value =0.0092), Interleukin-16 (coefficient =0.3949, P value =0.0435).ConclusionsWe investigated the genetic correlations between plasma proteins and different sites of OA in a systematic way. Our results provide novel evidence that OA is a heterogeneous disease.

Predictive power of the ADHD GWAS 2019 polygenic risk scores in independent samples of bipolar patients with childhood ADHD

BackgroundAlthough there is evidence of genetic correlation between bipolar disorder (BP) and ADHD, the extent of the shared genetic risk and whether childhood ADHD (cADHD) influences the characteristics of the adult BP remain unclear. Our objectives were: (i) to test the ability of polygenic risk scores (PRS) derived from the latest PGC ADHD-GWAS (Demontis et al., 2019) to predict the presence of cADHD in BP patients; (ii) to examine the hypothesis that BP preceded by cADHD is a BP subtype with particular clinical traits and (iii) partially shares its molecular basis with ADHD. MethodPRS derived from the ADHD-GWAS-2019 were tested in BP patients (N = 942) assessed for cADHD with the Wender Utah Rating Scale and in controls from Romania and UK (N = 1616). ResultsThe ADHD-PRS differentiated BP cases with cADHD from controls. Proband sex and BP age-of-onset significantly influenced the discriminative power of the ADHD-PRS. The ADHD-PRS predicted the cADHD score only in males and in BP cases with early age-of-onset (≤21 years). Bipolar patients with cADHD had a younger age-of-onset of mania/depression than patients without cADHD. The ADHD-PRS predicted the BP-affection status in the comparison of early-onset BP cases with controls suggesting a partial molecular overlap between early-onset BP and ADHD. LimitationsRetrospective diagnosis of cADHD, small sample size. ConclusionsThe PRS-analysis indicated an acceptable predictive ability of the ADHD-SNP-set 2019 in independent BP samples. The best prediction of both cADHD and BP-affection status was found in the early-onset BP cases. The results may have impact on the individual disease monitoring.

Evidence for genetic correlation between human cerebral white matter microstructure and inflammation.

White matter microstructure is affected by immune system activity via the actions of circulating pro-inflammatory cytokines. Although white matter microstructure and inflammatory measures are significantly heritable, it is unclear if overlapping genetic factors influence these traits in humans. We conducted genetic correlation analyses of these traits using randomly ascertained extended pedigrees from the Genetics of Brain Structure and Function Study (N = 1862, 59% females, ages 18-97 years; 42 ± 15.7). White matter microstructure was assessed using fractional anisotropy (FA) calculated from diffusion tensor imaging (DTI). Circulating levels (pg/mL) of pro-inflammatory cytokines (IL-6, IL-8, and TNFα) phenotypically associated with white matter microstructure were quantified from blood serum. All traits were significantly heritable (h2 ranging from 0.41 to 0.66 for DTI measures and from 0.18 to 0.30 for inflammatory markers). Phenotypically, higher levels of circulating inflammatory markers were associated with lower FA values across the brain (r = -.03 to r = -.17). There were significant negative genetic correlations between most DTI measures and IL-8 and TNFα, although effects for TNFα were no longer significant when covarying for body mass index. Genetic correlations between DTI measures and IL-6 were not significant. Understanding the genetic correlation between specific inflammatory markers and DTI measures may help researchers focus questions related to inflammatory processes and brain structure.

Evidence for Genetic Correlations and Bidirectional, Causal Effects Between Smoking and Sleep Behaviors.

IntroductionCigarette smokers are at increased risk of poor sleep behaviors. However, it is largely unknown whether these associations are due to shared (genetic) risk factors and/or causal effects (which may be bidirectional).MethodsWe obtained summary-level data of genome-wide association studies of smoking (smoking initiation [n = 74 035], cigarettes per day [n = 38 181], and smoking cessation [n = 41 278]) and sleep behaviors (sleep duration and chronotype, or “morningness” [n = 128 266] and insomnia [n = 113 006]). Using linkage disequilibrium (LD) score regression, we calculated genetic correlations between smoking and sleep behaviors. To investigate causal effects, we employed Mendelian randomization (MR), both with summary-level data and individual-level data (n = 333 581 UK Biobank participants). For MR with summary-level data, individual genetic variants were combined with inverse variance–weighted meta-analysis, weighted median regression, MR-Robust Adjusted Profile Score, and MR Egger methods.ResultsWe found negative genetic correlations between smoking initiation and sleep duration (rg = −.14, 95% CI = −0.26 to −0.01) and smoking cessation and chronotype (rg = −.18, 95% CI = −0.31 to −0.06), and positive genetic correlations between smoking initiation and insomnia (rg = .27, 95% CI = 0.06 to 0.49) and cigarettes per day and insomnia (rg = .15, 95% CI = 0.01 to 0.28). MR provided strong evidence that smoking more cigarettes causally decreases the odds of being a morning person, (RAPS) and weak evidence that insomnia causally increases smoking heaviness and decreases smoking cessation odds.ConclusionsSmoking and sleep behaviors show moderate genetic correlation. Heavier smoking seems to causally affect circadian rhythm and there is some indication that insomnia increases smoking heaviness and hampers cessation. Our findings point to sleep as a potentially interesting smoking treatment target.ImplicationsUsing LD score regression, we found evidence that smoking and different sleep behaviors (sleep duration, chronotype (morningness), and insomnia) are moderately genetically correlated—genetic variants associated with less or poorer sleep also increased the odds of smoking (more heavily). MR analyses suggested that heavier smoking causally affects circadian rhythm (decreasing the odds of being a morning person) and there was some indication that insomnia increases smoking heaviness and hampers smoking cessation. Our findings indicate a complex, bidirectional relationship between smoking and sleep behaviors and point to sleep as a potentially interesting smoking treatment target.

Independence of genetic variation between circadian rhythm and development time in the seed beetle, Callosobruchus chinensis

A positive genetic correlation between periods of circadian rhythm and developmental time supports the hypothesis that circadian clocks are implicated in the timing of development. Empirical evidence for this genetic correlation in insects has been documented in two fly species. In contrast, here we show that there is no evidence of genetic correlation between circadian rhythm and development time in the adzuki bean beetle, Callosobruchus chinensis. This species has variation that is explained by a major gene in the expression and period length of circadian rhythm between strains. In this study, we found genetic variation in development time between the strains. The development time was not covaried with either the incidence or the period length of circadian rhythm among the strains. Crosses between strains suggest that development time is controlled by a polygene. In the F2 individuals from the crosses, the circadian rhythm is attributable to allelic variation in the major gene. Across the F2 individuals, development time was not correlated with either the expression or the period length of circadian rhythm. Thus, we found no effects of major genes responsible for variation in the circadian rhythm on development time in C. chinensis. Our findings collectively give no support to the hypothesis that the circadian clock is involved in the regulation of development time in this species.

VARIANCES AND COVARIANCES OF PHENOLOGICAL TRAITS IN A WILD MAMMAL POPULATION

In a seasonal environment, there are multiple aspects of timing, or phenology, that contribute to an individual's fitness. Several studies have shown a genetic basis to variation between individuals in breeding time, but we know little about the heritability of other phenological traits in wild populations. Furthermore, the presence of genetic correlations between phenological variables could act to constrain or promote any response to selection, but less is known of the multivariate genetic relationships underlying phenological traits in the wild. Here, we use data from a wild population of red deer on the Isle of Rum, Scotland, to investigate covariances between eight phenological traits. Variation was characterized at the level of the phenotype, genotype, and year, and traits measured in different sexes enabled us to test for cross-sex genetic correlations. Phenotypic correlations were broadly strong and positive, as were correlations between traits expressed in the same year. We found evidence of significant additive genetic variation in five of the eight phenological traits studied. However there was little evidence of genetic correlations between traits, implying that much of the observed phenotypic correlation was environmentally induced. Our results suggest that different phenological traits may be free to move along independent evolutionary trajectories.

Colour polymorphism and correlated characters: genetic mechanisms and evolution

Colour polymorphisms (CP's) continue to be of interest to evolutionary biologists because of their general tractability, importance in studies of selection and potential role in speciation. Since some of the earliest studies of CP, it has been evident that alternative colour morphs often differ in features other than colour. Here we review the rapidly accumulating evidence concerning the genetic mechanisms underlying correlations between CP and other traits in animals. We find that evidence for genetic correlations is now available for taxonomically diverse systems and that physical linkage and regulatory mechanisms including transcription factors, cis-regulatory elements, and hormone systems provide pathways for the ready accumulation or modification of these correlations. Moreover, physical linkage and regulatory mechanisms may both contribute to genetic correlation in some of the best-studied systems. These results raise the possibility that negative frequency-dependent selection and disruptive selection might often be acting on suites of traits and that the cumulative effects of such selection, as well as correlational selection, may be important to CP persistence and evolution. We consider additional evolutionary implications. We recommend continued efforts to elucidate the mechanisms underlying CP-correlated characters and the more frequent application of comparative approaches, looking at related species that vary in character correlations and patterns of selection. We also recommend efforts to elucidate how frequency-dependent selection may act on suites of characters.

A survey of acute and chronic heroin dependence in ten inbred mouse strains: Evidence of genetic correlation with morphine dependence

Heroin and morphine exposure can cause physical dependence, with symptoms manifesting during their withdrawal. Inter-individual differences in symptom frequency during morphine withdrawal are a common finding that, in rodents, is demonstrably attributable to genotype. However, it is not known whether inter-individual differences characterize heroin withdrawal, and whether such variation can be similarly influenced by genotype. Therefore, we injected mice of ten inbred strains with acute and chronic heroin doses and compared their jumping frequencies, a common index of withdrawal magnitude, during naloxone-precipitated withdrawal. The data revealed significant strain frequency differences (range after acute and chronic heroin injection: 0–104 and 0–142 jumps, respectively) and substantial heritability ( h 2 = 0.94 to 0.96), indicating that genetic variance is associated with heroin withdrawal. The rank order of strain sensitivity for acute and chronic heroin withdrawal jumping, and for the current heroin and previous morphine strain data, were significantly correlated ( r = 0.75–0.94), indicating their genetic and, ultimately, physiological commonality. These data suggest that the genetic liability to heroin dependence remains constant across a period of heroin intake, and that heroin and morphine dependence may benefit from common treatment strategies.

Studies in quantitative inheritance. XI. Genetic and environmental correlation between body size and egg production in Drosophila melanogaster. 1957.

1. The variation of body size and egg production between individuals of a laboratory population ofDrosophila melanogaster has been examined. Estimates of genetic and environmental contributions to the phenotypic variation have been derivedby comparing the variability of the flies of the wild population with that of genetically uniform flies from crosses between inbred lines reared under similar favourable conditions. Apparently about 50 % of the variance of body size and about 60 % of the variance of egg production is attributable to genetic segregation. 2. From the results of two-way selection for body size and also egg production, the heritability of the two characters is estimated as respectively 0.43 and 0.18, suggesting that most of the genetic variation in body size behaves as additive in the statistical sense, while non-additive effects predominate in the variability of egg production. 3. There is a clear-cut phenotypic correlation between size and egg production among the individuals of the wild population and this is mostly genetic in origin. Selection for large and small size leads to comparatively little change in egg production. A series of different genotypes, each represented by a number of genetically identical individuals; were prepared by combining haploid sets of chromosomes from the wild population with a haploid set from an inbred line—and these provided no evidence of genetic correlation between size and egg production. Hence the genetic correlation in the wild stock is essentially non-additive in behaviour. 4. Gene-environment interaction has been demonstrated for both egg production and body size by comparing estimates of variance and heritability on the live medium with those found on a synthetic medium which permits normal growth. It is suggested that gene-environment interaction will be particularly important under the suboptimal condition in which the population usually lives. 5. Reduction of the body size of genetically uniform flies by varying the nutrition of the larvae leads to a proportional reduction in the rate at which eggs are laid. 6. The variability of development time has also been examined in preliminary experiments which indicate that about half the variance is genetic in origin. Under favourable conditions there is a high correlation between length of development and body size, while egg production tends to be negatively correlated, suggesting that egg production and growth rate are genetically associated. 7. The results are discussed in relation to the stability of average body size in. the population and the ease with which selection either way leads to striking change. There are strong indications that the apparently continuous variation of attributes such as size or egg production are heterogeneous with respect to the effects on physiology and development which contribute to the final variation, while the relative contribution of different sorts of effect may vary according to environmental conditions.

Ecological genetics of an induced plant defense against herbivores: additive genetic variance and costs of phenotypic plasticity.

Adaptive phenotypic plasticity in chemical defense is thought to play a major role in plant-herbivore interactions. We investigated genetic variation for inducibility of defensive traits in wild radish plants and asked if the evolution of induction is constrained by costs of phenotypic plasticity. In a greenhouse experiment using paternal half-sibling families, we show additive genetic variation for plasticity in glucosinolate concentration. Genetic variation for glucosinolates was not detected in undamaged plants, but was significant following herbivory by a specialist herbivore, Pieris rapae. On average, damaged plants had 55% higher concentrations of glucosinolates compared to controls. In addition, we found significant narrow-sense heritabilities for leaf size, trichome number, flowering phenology, and lifetime fruit production. In a second experiment, we found evidence of genetic variation in induced plant resistance to P. rapae. Although overall there was little evidence for genetic correlations between the defensive and life-history traits we measured, we show that more plastic families had lower fitness than less plastic families in the absence of herbivory (i.e., evidence for genetic costs of plasticity). Thus, there is genetic variation for induction of defense in wild radish, and the evolution of inducibility may be constrained by costs of plasticity.

ECOLOGICAL GENETICS OF AN INDUCED PLANT DEFENSE AGAINST HERBIVORES: ADDITIVE GENETIC VARIANCE AND COSTS OF PHENOTYPIC PLASTICITY

Adaptive phenotypic plasticity in chemical defense is thought to play a major role in plant-herbivore interactions. We investigated genetic variation for inducibility of defensive traits in wild radish plants and asked if the evolution of induction is constrained by costs of phenotypic plasticity. In a greenhouse experiment using paternal half-sibling families, we show additive genetic variation for plasticity in glucosinolate concentration. Genetic variation for glucosinolates was not detected in undamaged plants, but was significant following herbivory by a specialist herbivore, Pieris rapae. On average, damaged plants had 55% higher concentrations of glucosinolates compared to controls. In addition, we found significant narrow-sense heritabilities for leaf size, trichome number, flowering phenology, and lifetime fruit production. In a second experiment, we found evidence of genetic variation in induced plant resistance to P. rapae. Although overall there was little evidence for genetic correlations between the defensive and life-history traits we measured, we show that more plastic families had lower fitness than less plastic families in the absence of herbivory (i.e., evidence for genetic costs of plasticity). Thus, there is genetic variation for induction of defense in wild radish, and the evolution of inducibility may be constrained by costs of plasticity.

The Relationship Between Ethanol‐induced Hyperglycemia and Hypothermia: Evidence of Genetic Correlation

The hyperglycemic and hypothermic responses to acute ethanol exposure (0, 2, 4, 6 g/kg, intraperitoneally) were examined in non-fasted mice selectively bred for sensitivity (COLD line) or insensitivity (HOT line) to ethanol-induced hypothermia. Blood samples and rectal temperatures were obtained immediately before injection and hourly for 4 hr after injection. As expected, COLD mice demonstrated greater and more prolonged reductions in body temperature than HOT mice, especially at the 4 g/kg dose (HOT: -2.58 degrees C, COLD: -5.08 degrees C). Ethanol produced significant dose-dependent elevations in blood glucose levels over the 4-hr sampling period in both lines. The greatest elevations in blood glucose levels were seen at 4 g/kg, with COLD mice (mean = 225.1 mg/dl) showing significantly greater elevations in blood glucose levels compared to HOT mice (mean = 177.0 mg/dl). These results support the hypothesis that the thermic and glycemic effects produced by ethanol are due to related neural processes that share a common genetic component.

A Replicated Test for Correlated Responses in Egg Weight and Early Growth Rate from Selection for Hatching Time in the Fowl

Selection for fast and slow hatching time for a single generation in five replicates resulted in significant direct responses in hatching time. The realized heritability estimates varied from .10 to .34 over replicates with a mean value of .19 ± .02. No significant correlated responses were observed in embryo weight at 14 days of incubation or in chick body weight at hatching, measured on the progeny of the selected parents for the first generation. Previous results in single replicate experiments where a theoretical estimate of the random genetic drift error was used in the tests, indicated significant correlated responses in embryo and chick weight. It is suggested that replicated experiments such as the present one provide an empirical estimate of the error including random genetic drift which would be more accurate as a tester for line differences. No significant differences between the selected lines were observed for egg weight, adult body weight, age at 50% production, rate of lay, or hatchability when these means were measured on the selected parents. It is concluded that there is no evidence of genetic correlations between hatching time and any of the other traits measured in the egg production strains studied.