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Genetic variation in offspring indirectly influences the quality of maternal behaviour in mice.

ABSTRACT: Conflict over parental investment between parent and offspring is predicted to lead to selection on genes expressed in offspring for traits influencing maternal investment, and on parentally expressed genes affecting offspring behaviour. However, the specific genetic variants that indirectly modify maternal or offspring behaviour remain largely unknown. Using a cross-fostered population of mice, we map maternal behaviour in genetically uniform mothers as a function of genetic variation in offspring and identify loci on offspring chromosomes 5 and 7 that modify maternal behaviour. Conversely, we found that genetic variation among mothers influences offspring development, independent of offspring genotype. Offspring solicitation and maternal behaviour show signs of coadaptation as they are negatively correlated between mothers and their biological offspring, which may be linked to costs of increased solicitation on growth found in our study. Overall, our results show levels of parental provisioning and offspring solicitation are unique to specific genotypes.

SUBMITTER: Ashbrook DG

PROVIDER: S-EPMC4758942 | biostudies-literature | 2015 Dec

REPOSITORIES: biostudies-literature

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Genetic variation in offspring indirectly influences the quality of maternal behaviour in mice.

Ashbrook David George DG Gini Beatrice B Hager Reinmar R

eLife 20151223

Conflict over parental investment between parent and offspring is predicted to lead to selection on genes expressed in offspring for traits influencing maternal investment, and on parentally expressed genes affecting offspring behaviour. However, the specific genetic variants that indirectly modify maternal or offspring behaviour remain largely unknown. Using a cross-fostered population of mice, we map maternal behaviour in genetically uniform mothers as a function of genetic variation in offspr ...[more]

PMID: 26701914

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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.

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-1β 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.

Dataset Information

Genetic variation in offspring indirectly influences the quality of maternal behaviour in mice.

Publications

Genetic variation in offspring indirectly influences the quality of maternal behaviour in mice.

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