Genetic variation in offspring indirectly influences the quality of maternal behaviour in mice.
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ABSTRACT:
SUBMITTER: Ashbrook DG
PROVIDER: S-EPMC4758942 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Aims/hypothesisDuring pregnancy, maternal metabolic disease and hormonal imbalance may alter fetal beta cell development and/or proliferation, thus leading to an increased risk for developing type 2 diabetes in adulthood. Although thyroid hormones play an important role in fetal endocrine pancreas development, the impact of maternal hypothyroidism on glucose homeostasis in adult offspring remains poorly understood.MethodsWe investigated this using a mouse model of hypothyroidism, induced by administration of an iodine-deficient diet supplemented with propylthiouracil during gestation.ResultsHere, we show that, when fed normal chow, adult mice born to hypothyroid mothers were more glucose-tolerant due to beta cell hyperproliferation (two- to threefold increase in Ki67-positive beta cells) and increased insulin sensitivity. However, following 8 weeks of high-fat feeding, these offspring gained 20% more body weight, became profoundly hyperinsulinaemic (with a 50% increase in fasting insulin concentration), insulin-resistant and glucose-intolerant compared with controls from euthyroid mothers. Furthermore, altered glucose metabolism was maintained in a second generation of animals.Conclusions/interpretationTherefore, gestational hypothyroidism induces long-term alterations in endocrine pancreas function, which may have implications for type 2 diabetes prevention in affected individuals.
| S-EPMC7406527 | biostudies-literature
Project description:Family members show behavioural strategies predicted to maximize individual fitness. These behaviours depend directly on genes expressed in focal individuals but also indirectly on genes expressed in other family members. However, how sibling and parental behavioural strategies are modified by genes expressed in family members, and to what degree, remains unclear. To answer this question, we have used a split litter design in an experimental population of genetically variable mouse families, and identified loci that indirectly affected sibling and maternal behaviour simultaneously. These loci map to genomic regions that also show a direct effect on offspring behaviour. Directly and indirectly affected traits were significantly correlated at the phenotypic level, illustrating how indirect effects are caused. Genetic variants in offspring that influence solicitation also impacted their siblings' and maternal behaviour. However, in contrast to predictions from sibling competition, unrelated litter mates benefited from increased solicitation. Overall, such indirect genetic effects explained a large proportion of variation seen in behaviours, with candidate genes involved in metabolism to neuronal development. These results reveal that we need to view behavioural strategies as the result of conjoint selection on genetic variation in all interacting family members.
| S-EPMC5627198 | biostudies-literature
Project description:Ectopic mineralization disorders inflicting the connective tissues display a spectrum of severity, some developing in utero and being diagnosed by prenatal ultrasound. This study was designed to test the hypothesis that the mineral content of maternal diet can influence the mineralization in the offspring. Pregnant Abcc6(-/-) mice, on 2 different strain backgrounds, were maintained either on normal rodent diet or on "acceleration diet," rich in phosphate and low in magnesium, which has been previously shown to enhance the mineralization processes. The offspring were examined for mineralization by histopathology of various tissues and quantitated by chemical assay of calcium. The ectopic mineralization in the dermal sheath of vibrissae, a progressive biomarker of the overall mineralization, was readily detectable at the age of 4 weeks in the pups whose mothers were on the acceleration diet, while no evidence of mineralization was noted in those on normal diet. The mineralization of the vibrissae progressively increased when examined at 12 weeks of age. There was a significant reduction in urinary calcium and significant increase in urinary phosphorus concentrations both at 4 and 12 weeks of age in mice on the acceleration diet as compared to those on control diet. The results demonstrate that the mineral content of the maternal diet can influence ectopic mineralization in the offspring of mice genetically predisposed to ectopic mineralization (Abcc6(-/-)). These observations have implications for dietary management of pregnancies in which the fetus is diagnosed by prenatal ultrasound to have an ectopic mineralization disorder.
| S-EPMC4825565 | biostudies-literature
Project description:This study aimed to investigate the effects of maternal dietary coated methionine (Met) on egg production and the quality, growth performance, carcass traits, and meat quality of the offspring. In total, 288 female Ross parental chickens were randomly assigned to 3 groups with 3 replicates of 32 chickens each. From week 37 to 46, the hens of different groups were fed diets containing low (0.27% Met), adequate (0.27% Met + 0.1% coated Met) (AM), and high (0.27% Met + 0.2% coated Met) (HM) Met. There was a positive response in laying rate and albumen weight in AM and HM groups. For the offspring at market age, BW, eviscerated weight, and muscle weight were increased in the AM group (P < 0.05), whereas excessive supplementation was proven to be negative with those traits. The meat quality (color, pH, and shear force) of breast muscle was significantly influenced by different supplementation levels. The lightness and yellowness were increased in the HM group (P < 0.05, P < 0.01, respectively), and redness was decreased in the AM group (P < 0.05). A lower pH value occurred in chickens of the HM group (P < 0.05). The expressions of meat quality-related genes were altered in the supplementation groups. The pH-related genes PRDX4 and PRKAG2 were found to be significantly differentially expressed (P < 0.05, P < 0.01, respectively) and consistent with pH changes. The meat color-related gene BCO1 was also differentially expressed (P < 0.01) and showed a corresponding change with yellowness value. Collectively, the best production performance was in the offspring with 0.1% coated Met supplementation (AM group). Supplementation with 0.2% coated Met (HM group) seemed to be excessive, but laying rate was increased in the HM group. Both results of phenotypic measurements and gene expression demonstrated that maternal-coated Met supplementation resulted in fluctuation of some meat quality indices in the offspring, but all values were still within the range found in normal chickens.
| S-EPMC7597828 | biostudies-literature
Project description:Congenital heart defects (CHDs) are among the most prevalent and serious birth defects, occurring in 8 to 10 of every 1000 live births in the United States. Epidemiologic studies have reported an association between CHDs and maternal smoking, but it remains unknown how genes impact the susceptibility of offspring to CHDs in the presence of maternal tobacco use.Using data from 403 case- and 219 control-parental triads enrolled in the National Birth Defects Prevention Study between 1998 and 2008, we investigated the association between CHDs and maternal and infant genetic variants involved in the tobacco metabolism and DNA repair pathways among mothers who smoked prenatally.The maternal genotypes of single nucleotide polymorphisms in the excision repair cross-complementation group 1 (ERCC1), poly (ADP-ribose) polymerase 2 (PARP2), and ERCC5 genes were identified to be significantly associated with the occurrence of CHDs in the presence of maternal tobacco use. Our analysis also revealed a moderate association between the infant genotypes of polymorphisms in the O-sialoglycoprotein endopeptidase (OSGEP) gene and increased risk of CHDs among mothers who smoked.Our study provides evidence that maternal and infant polymorphisms within the ERCC1, PARP2, ERCC5, and OSGEP genes are associated with CHD risk in the presence of maternal tobacco use. These results may provide insight into the susceptibility of having a pregnancy affected by CHDs among women who smoke.
| S-EPMC4774247 | biostudies-literature
Project description:BackgroundMaternal pre-pregnancy body-mass index (ppBMI) and gestational weight gain (GWG) are associated with cardiometabolic risk (CMR) traits in the offspring. The extent to which maternal genetic variation accounts for these associations is unknown.Methods/resultsIn 1249 mother-offspring pairs recruited from the Jerusalem Perinatal Study, we used archival data to characterize ppBMI and GWG and follow-up data from offspring to assess CMR, including body mass index (BMI), waist circumference, glucose, insulin, blood pressure, and lipid levels, at an average age of 32. Maternal genetic risk scores (GRS) were created using a subset of SNPs most predictive of ppBMI, GWG, and each CMR trait, selected among 1384 single-nucleotide polymorphisms (SNPs) characterizing variation in 170 candidate genes potentially related to fetal development and/or metabolic risk. We fit linear regression models to examine the associations of ppBMI and GWG with CMR traits with and without adjustment for GRS. Compared to unadjusted models, the coefficient for the association of a one-standard-deviation (SD) difference in GWG and offspring BMI decreased by 41% (95%CI -81%, -11%) from 0.847 to 0.503 and the coefficient for a 1SD difference in GWG and WC decreased by 63% (95%CI -318%, -11%) from 1.196 to 0.443. For other traits, there were no statistically significant changes in the coefficients for GWG with adjustment for GRS. None of the associations of ppBMI with CMR traits were significantly altered by adjustment for GRS.ConclusionsMaternal genetic variation may account in part for associations of GWG with offspring BMI and WC in young adults.
| S-EPMC3966761 | biostudies-literature
Project description:Like most ectothermic vertebrates, keelback snakes (Tropidonophis mairii) do not exhibit parental care. Thus, offspring must possess an immune system capable of dealing with challenges such as pathogens, without assistance from an attendant parent. We know very little about immune system characteristics of neonatal reptiles, including the magnitude of heritability and other maternal influences. To identify sources of variation in circulating white blood cell (WBC) concentrations and differentials, we examined blood smears from 246 hatchling snakes and their field-caught mothers. WBC concentrations were lower in hatchlings than in adults, and hatchlings had more basophils and fewer azurophils than adults. A hatchling keelback's WBC differential was also influenced by its sex and body size. Although hatchling WBC measures exhibited negligible heritability, they were strongly influenced by maternal body size and parasite infection (but not by maternal body condition, relative clutch mass or time in captivity). Larger mothers produced offspring with more azurophils and fewer lymphocytes. The mechanisms and consequences of WBC variation are currently unknown, but if these maternal effects enhance offspring fitness, the impact of maternal body size on reproductive success may be greater than expected simply from allometric increases in the numbers and sizes of progeny.
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Project description:Adverse experiences during pregnancy induce placental programming, affecting the fetus and its developmental trajectory. However, the influence of 'positive' maternal experiences on the placenta and fetus remain unclear. In animal models of early life stress, environmental enrichment (EE) has ameliorated and even prevented associated impairments in brain and behavior. Here, using a maternal immune activation (MIA) model in rats, we test whether EE attenuates maternal, placental and/or fetal responses to an inflammatory challenge, thereby offering a mechanism by which fetal programming may be prevented. Moreover, we evaluate life-long EE exposure on offspring development and examine a constellation of genes and epigenetic writers that may protect against MIA challenges. In our model, maternal plasma corticosterone and interleukin-1? were elevated 3?h after MIA, validating the maternal inflammatory response. Evidence for developmental programming was demonstrated by a simultaneous decrease in the placental enzymes Hsd11b2 and Hsd11b2/Hsd11b1, suggesting disturbances in glucocorticoid metabolism. Reductions of Hsd11b2 in response to challenge is thought to result in excess glucocorticoid exposure to the fetus and altered glucocorticoid receptor expression, increasing susceptibility to behavioral impairments later in life. The placental, but not maternal, glucocorticoid implications of MIA were attenuated by EE. There were also sustained changes in epigenetic writers in both placenta and fetal brain as a consequence of environmental experience and sex. Following MIA, both male and female juvenile animals were impaired in social discrimination ability. Life-long EE mitigated these impairments, in addition to the sex specific MIA associated disruptions in central Fkbp5 and Oprm1. These data provide the first evidence that EE protects placental functioning during stressor exposure, underscoring the importance of addressing maternal health and well-being throughout pregnancy. Future work must evaluate critical periods of EE use to determine if postnatal EE experience is necessary, or if prenatal exposure alone is sufficient to confer protection.
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Project description:Evolutionary models of sex ratio adjustment applied to mammals have ignored that females may gain indirect genetic benefits from their mates. The differential allocation hypothesis (DAH) predicts that females bias the sex ratio of their offspring towards (more costly) males when breeding with an attractive male. We manipulated the number of available males during rut in a polygynous ungulate species, the reindeer (Rangifer tarandus), and found that a doubling of average male mass (and thus male attractiveness) in the breeding herd increased the proportion of male offspring from approximately 40 to 60%. Paternity analysis revealed indeed that males of high phenotypic quality sired more males, consistent with the DAH. This insight has consequences for proper management of large mammal populations. Our study suggests that harvesting, by generating a high proportion of young, small and unattractive mates, affects the secondary sex ratio due to differential allocation effects in females. Sustainable management needs to consider not only the direct demographic changes due to harvest mortality and selection, but also the components related to behavioural ecology and opportunities for female choice.
| S-EPMC2197213 | biostudies-literature
Project description:Close interactions between mother and offspring are said to result in a coevolution of parental and offspring genotypes such that offspring are adapted in their solicitation behaviour to obtain maternal provisioning that maximizes their fitness. Few empirical studies have been conducted in this field and it remains unclear whether maternal provisioning and offspring weight gain are influenced by the same set of maternal and offspring phenotypic and genotypic factors. Using a cross-foster, split-litter design in mice, we found that overall maternal provisioning and offspring weight gain are significantly correlated but are affected by a different set of parameters, except for the effect of maternal bodyweight. While the level of maternal provisioning was influenced by both offspring and foster mother genotype, offspring weight gain was only affected by the number of males in the mixed litter. We suggest that this disparity may hint at the inefficiency of offspring solicitation behaviour or effects of sibling competition.
| S-EPMC1617205 | biostudies-literature