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The influence of phenotypic and genetic effects on maternal provisioning and offspring weight gain in mice.

ABSTRACT: 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.

SUBMITTER: Hager R

PROVIDER: S-EPMC1617205 | biostudies-literature | 2006 Mar

REPOSITORIES: biostudies-literature

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The influence of phenotypic and genetic effects on maternal provisioning and offspring weight gain in mice.

Hager Reinmar R Johnstone Rufus A RA

Biology letters 20060301 1

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- ...[more]

PMID: 17148332

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Project description:Maternal nutrition during pregnancy influences postnatal life of animals; nevertheless, few studies have investigated its effects on the productive performance and reproductive development of heifers. This study evaluated the performance, reproductive development, and correlation between reproduction × fat thickness and performance × ribeye area (REA) traits of heifers. We also performed an exploratory genomic association during the rearing period in heifers submitted to fetal programming. The study comprised 55 Nellore heifers born to dams exposed to one of the following nutritional planes: control, without protein-energy supplementation; PELT, protein-energy last trimester, protein-energy supplementation offered in the final third of pregnancy; and PEWG, protein-energy whole gestation, protein-energy supplementation upon pregnancy confirmation. Protein-energy supplementation occurred at the level of 0.3% live weight. After weaning, heifers were submitted to periodic evaluations of weight and body composition by ultrasonography. From 12 to 18 months, we evaluated the reproductive tract of heifers to monitor its development for sexual precocity and ovarian follicle population. The treatments had no effect (p > 0.05) on average daily gain; however, the weight of the animals showed a significant difference over time (p = 0.017). No differences were found between treatments for REA, backfat, and rump fat thickness, nor for puberty age, antral follicular count, and other traits related to reproductive tract development (p > 0.05). The correlation analysis between performance traits and REA showed high correlations (r > 0.37) between REA at weaning and year versus weight from weaning until yearling; however, no correlation was found for reproductive development traits versus fat thickness (p > 0.05). The exploratory genomic association study showed one single-nucleotide polymorphism (SNP) for each treatment on an intergenic region for control and PEWG, and the one for PELT on an intronic region of RAPGEF1 gene. Maternal nutrition affected only the weight of the animals throughout the rearing period.

Project description:BackgroundClinical recommendations to limit gestational weight gain (GWG) imply high GWG is causally related to adverse outcomes in mother or offspring, but GWG is the sum of several inter-related complex phenotypes (maternal fat deposition and vascular expansion, placenta, amniotic fluid and fetal growth). Understanding the genetic contribution to GWG could help clarify the potential effect of its different components on maternal and offspring health. Here we explore the genetic contribution to total, early and late GWG.Participants and methodsA genome-wide association study was used to identify maternal and fetal variants contributing to GWG in up to 10 543 mothers and 16 317 offspring of European origin, with replication in 10 660 mothers and 7561 offspring. Additional analyses determined the proportion of variability in GWG from maternal and fetal common genetic variants and the overlap of established genome-wide significant variants for phenotypes relevant to GWG (for example, maternal body mass index (BMI) and glucose, birth weight).ResultsApproximately 20% of the variability in GWG was tagged by common maternal genetic variants, and the fetal genome made a surprisingly minor contribution to explain variation in GWG. Variants near the pregnancy-specific beta-1 glycoprotein 5 (PSG5) gene reached genome-wide significance (P=1.71 × 10-8) for total GWG in the offspring genome, but did not replicate. Some established variants associated with increased BMI, fasting glucose and type 2 diabetes were associated with lower early, and higher later GWG. Maternal variants related to higher systolic blood pressure were related to lower late GWG. Established maternal and fetal birth weight variants were largely unrelated to GWG.ConclusionsWe found a modest contribution of maternal common variants to GWG and some overlap of maternal BMI, glucose and type 2 diabetes variants with GWG. These findings suggest that associations between GWG and later offspring/maternal outcomes may be due to the relationship of maternal BMI and diabetes with GWG.

Dataset Information

The influence of phenotypic and genetic effects on maternal provisioning and offspring weight gain in mice.

Publications

The influence of phenotypic and genetic effects on maternal provisioning and offspring weight gain in mice.

Similar Datasets

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