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90 results for “maternal stress”
Data and code for: Viviparous mothers impose stronger glucocorticoid‐mediated maternal stress effects on their offspring than oviparous mothers
<p><strong>Data and code accompanying the manuscript "Viviparous mothers impose stronger glucocorticoid‐mediated maternal stress effects on their offspring than oviparous mothers", MacLeod KJ, While GM, Uller, T, Ecology & Evolution 2021.</strong></p> <p>Code is in an R file - can be opened with any txt app.</p> <p>Metadata is in sheet 2 of the main data sheet (xlsx).</p> <p>Queries to kirstyjmacleod@gmail.com</p> <p><strong>Publication abstract</strong>: Maternal stress during gestation has the potential to affect offspring development via changes in maternal physiology, such as increases in circulating levels of glucocorticoid hormones that are typical after exposure to a stressor. While the effects of elevated maternal glucocorticoids on offspring phenotype (i.e., “glucocorticoid‐mediated maternal effects”) have been relatively well established in laboratory studies, it remains poorly understood how strong and consistent such effects are in natural populations. Using a meta‐analysis of studies of wild mammals, birds, and reptiles, we investigate the evidence for effects of elevated maternal glucocorticoids on offspring phenotype and investigate key moderators that might influence the strength and direction of these effects. In particular, we investigate the potential importance of reproductive mode (viviparity vs. oviparity). We show that glucocorticoid‐mediated maternal effects are stronger, and likely more deleterious, in mammals and viviparous squamate reptiles compared with birds, turtles, and oviparous squamates. No other moderators (timing and type of manipulation, age at offspring measurement, or type of trait measured) were significant predictors of the strength or direction of the phenotypic effects on offspring. These results provide evidence that the evolution of a prolonged physiological association between embryo and mother sets the stage for maladaptive, or adaptive, prenatal stress effects in vertebrates driven by glucocorticoid elevation.</p>
Data from: Maternal oxidative stress and reproduction: testing the constraint, cost and shielding hypotheses in a wild mammal
1. Oxidative stress has been proposed as a central causal mechanism underlying the life history trade-off between current and future reproduction and survival in wild animals. 2. Whereas mixed evidence suggests that maternal oxidative stress may act both as a constraint and a cost to reproduction, some studies have reported a lack of association between reproduction and maternal oxidative stress. 3. The oxidative shielding hypothesis offers an alternative explanation, suggesting that mothers may pre-emptively mitigate the oxidative costs of reproduction by increasing antioxidant defences prior to reproduction. 4. We tested the oxidative constraint, cost, and shielding hypotheses using a longitudinal field study of oxidative stress levels in a species that breeds using daily energy income, the Columbian ground squirrel (Urocitellus columbianus). 5. Elevated maternal oxidative damage prior to reproduction was associated with higher maternal investment in litter mass at birth, but not at weaning. 6. Breeding females increased their antioxidant capacity and decreased their oxidative damage from birth to lactation compared to non-breeding females measured at the same time periods. However, lower maternal oxidative stress during lactation was not associated with higher offspring survival or mass growth over this period. 7. Our results provide little evidence for maternal oxidative stress acting as a constraint on, or cost to, reproduction in Columbian ground squirrels, but partially support the idea that oxidative shielding occurred to buffer potential oxidative costs of reproduction.
Data of the study of Maternal temperature stress modulates acclimation and thermal biology in Octopus maya (Cephalopoda: Octopodidae) juvenile progeny
<p>These data shows the effects of temperature and exposure time on octopus juveniles obtained from thermal-stressed (30°C) and non-stressed (24°C) females when exposed to optimal (25°C) and high temperatures (30°C) for 20 and 30 days, respectively. Data of survival, and oxygen consumption (MR) were obtained, also in routine (RMR) and resting conditions (SMR). The high metabolic rate (HMR) was used to obtain the thermal metabolic scope (TMS) That was defined as: TMS = HMR - SMR<br> Data on the antioxidant defense enzymes and radical oxygen species (ROS) were used to evaluate if transgenerational effect of temperature provoked changes in the hability of juveniles to neutralize ROS. </p>
When ancestors transmit their stress: Prenatal maternal stress transmission across generations in a precocial bird
<p>Prenatal maternal stress (PMS) induces life-long effects in offspring. Accumulating evidence suggests that these effects can be transmitted across generations. Although multigenerational effects (F0 mother to F2 grand-offspring) of PMS have been demonstrated in different species, transgenerational transmission (F0 mother to F3 great-grand-offspring) has been less explored. We showed previously in the Japanese quail that PMS increased F1 offspring's emotional reactivity related to epigenetic marks levels in their brain and to modulation of testosterone concentrations in eggs from which they hatched. Here, we evaluated the multi- and transgenerational effects of PMS by analysing the emotional reactivity of the F2 and the F3 offspring. We also investigated the mechanisms potentially involved in the transmission of PMS across generations by analysing the hormonal composition of F1 and F2 eggs and by studying histone post-translational modifications in F3 brains. We showed that PMS increased the neophobia of F2 offspring and F3 females' offspring. We also observed modulations of androgens levels in F1 and F2 eggs but no modifications of the level of histone post-translational modification in F3 brains. Although the mechanisms involved in PMS transmission still need to be explored, our results demonstrate a multi- and transgenerational behavioural effect of PMS in birds.</p>
When ancestors transmit their stress: Prenatal maternal stress transmission across generations in a precocial bird
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Data from: Maternal oxidative stress and reproduction: testing the constraint, cost and shielding hypotheses in a wild mammal
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Data from: Environmental stress linked to consumption of maternally derived carotenoids in brown trout embryos (Salmo trutta)
The yellow, orange, or red colors of salmonid eggs are due to maternally derived carotenoids whose functions are not sufficiently understood yet. Here, we studied the significance of naturally acquired carotenoids as maternal environmental effects during embryo development in brown trout (Salmo trutta). We collected eggs from wild females, quantified their egg carotenoid content, fertilized them in vitro in full-factorial breeding blocks to separate maternal from paternal effects, and raised 3,278 embryos singly at various stress conditions until hatching. We found significant sire effects that revealed additive genetic variance for embryo survival and hatching time. Dam effects were 5.4 times larger than these sire effects, indicating that maternal environmental effects play an important role in determining embryo stress tolerance. Of the eight pigment molecules that we targeted, only astaxanthin, zeaxanthin (that both affected egg redness), and lutein were detected above our confidence thresholds. No strong link could be observed between carotenoid content in unfertilized eggs and embryo mortality or hatching timing. However, the consumption of carotenoids during our stress treatment was negatively correlated to embryo survival among sib groups and explained about 14% of the maternal environmental variance. We conclude that maternally derived carotenoids play a role in the ability of embryos to cope with environmental stress, but that the initial susceptibility to the organic pollution was mainly determined by other factors.
The prenatal hypoxic pathology associated with maternal stress predisposes to dysregulated expression of the chrna7 gene and the subsequent development of nicotine addiction in adult offspring (Supplementary)
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Maternal, Adiposity, Metabolism, and Stress Study
ClinicalTrials.gov study NCT01307683. IPD Sharing: Not stated. Countries: 1. Publications: 4.
Impact of Early Intervention on Maternal Stress in Mothers of Fetuses Diagnosed With Single Ventricle Physiology
ClinicalTrials.gov study NCT02462434. IPD Sharing: Not stated. Countries: 1. Publications: 16.
The Effect of Mother-Baby Yoga Baby Perception, Maternal Attachment,Depression-Anxiety-Stress
ClinicalTrials.gov study NCT06202937. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Prenatal Intervention of Maternal Stress - Breastfeeding & Infant Neurodevelopment
ClinicalTrials.gov study NCT06876051. IPD Sharing: NO. Countries: 1. Publications: 31.
Evaluating Pathophysiological Mechanisms of Acute and Chronic Heat Stress on Maternal and Fetal Health
ClinicalTrials.gov study NCT07326176. IPD Sharing: NO. Countries: 1. Publications: 2.
Kangaroo Holding and Maternal Stress
ClinicalTrials.gov study NCT00271115. IPD Sharing: Not stated. Countries: 1. Publications: 3.
Fetal Biomarkers of Chronic Maternal Stress During Pregnancy
ClinicalTrials.gov study NCT03389178. IPD Sharing: Not stated. Countries: 1. Publications: 2.
Data from: Environmental stress linked to consumption of maternally derived carotenoids in brown trout embryos (Salmo trutta)
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Data from: Transcriptome profiling of maternal stress-induced wing dimorphism in pea aphids
Wing dimorphism, i.e., wingless and winged forms, can be induced by maternal stress signals and is an adaptive response of aphids to environmental changes. Here, we investigated the ecological and molecular effects of three kinds of stress, namely, crowding, predation, and aphid alarm pheromone, on wing dimorphism. These three stressors induced high proportion of up to 60% of winged morphs in offspring. Transcriptome analysis of stress-treated female aphids revealed different changes in maternal gene expression as induced by the three stressors. Crowding elicited widespread changes in the expression of genes involved in nutrient accumulation and energy mobilization. Distinct from crowding, predation caused dramatic expression changes in cuticle protein (CP) genes. Twenty-three CP genes that belong to CP RR2 subfamily and are highly expressed in legs and embryos were greatly repressed by the presence of ladybird. By contrast, application of alarm pheromone, E--farnesene, caused slight changes in gene expression. The three factors shared a responsive gene, cuticle protein 43. This study reveals the adaptive response of aphids to environmental stresses and provides a rich resource on genome-wide expression genes for exploring molecular mechanisms of ecological adaptation in aphids.
Data from: Epistasis and maternal effects in experimental adaptation to chronic nutritional stress in Drosophila
Based on ecological and metabolic arguments some authors predict that adaptation to novel, harsh environments should involve alleles showing negative (diminishing return) epistasis and/or that it should be mediated in part by evolution of maternal effects. While the first prediction has been supported in microbes, there has been little experimental support for either prediction in multicellular eukaryotes. Here we use a line-cross design to study the genetic architecture of adaptation to chronic larval malnutrition in a population of Drosophila melanogaster which evolved on an extremely nutrient-poor larval food for 84 generations. We assayed three fitness-related traits (developmental rate, adult female weight and egg-to-adult viability) under the malnutrition conditions in 14 crosses between this selected population and a non-adapted control population originally derived from the same base population. All traits showed a pattern of negative epistasis between alleles improving performance under malnutrition. Furthermore, evolutionary changes in maternal traits accounted for half of the 68 % increase in viability and for the whole of 8 % reduction in adult female body weight in the selected population (relative to unselected controls). These results thus support both of the above predictions and point to the importance of non-additive effects in adaptive microevolution.
Data from: Maternal stress has divergent effects on gene expression patterns in the brains of male and female threespine stickleback
Maternal stress can have long-term effects on neurodevelopment that can influence offspring performance and population evolutionary trajectories. To examine the mechanistic basis for these neurodevelopmental effects of maternal stress, we used RNA-seq to assess differential gene expression across the brain transcriptome of adult male and female threespine stickleback (Gasterosteus aculeatus) from stressed and unstressed mothers. We identified sexually divergent effects of maternal stress on the brain transcriptome. In males, genes that were up-regulated by maternal stress were enriched for processes involved in synaptic function and organization and steroid hormone mediated signaling pathways, whereas in females genes that were up-regulated by maternal stress were enriched for processes involved in protein translation and metabolic functions. The expression of several genes involved in the hypothalamic-pituitary-interrenal response to stress and epigenetic processes such as the regulation of DNA methylation patterns and miRNAs increased in males and not in females. These data suggest that maternal stress has markedly different effects on cellular pathways in the brains of male and female offspring of mothers that are exposed to stress, which could have important implications when assessing the long-term ecological and evolutionary impacts of stress across generations.
Data from: Pre- and post-natal effects of experimentally manipulated maternal corticosterone on growth, stress reactivity, and survival of nestling house wrens
1. Corticosterone plays a central role in maintaining homeostasis, promoting energy acquisition, and regulating the stress response in birds. Exposure to elevated levels of corticosterone during development can profoundly alter offspring behaviour and physiology, but the effects of elevated maternal corticosterone on offspring development remain poorly understood. 2. We tested two competing hypotheses concerning the effect of maternally derived corticosterone on growth and development of free-living house wrens: i) elevated maternal corticosterone causes damaging effects on nestling phenotype and fitness (collateral damage hypothesis) and (ii) increased maternal corticosterone enhances offspring fitness by preparing nestlings for the environment experienced by their mother (environmental/maternal-matching hypothesis). 3. We used a non-invasive means to increase maternal corticosterone by providing females with corticosterone-injected mealworms prior to and during egg production in the absence of any overt pre-natal maternal stress. To disentangle pre- and post-natal effects of this elevation in maternal corticosterone, we cross-fostered young in two experiments: i) nestlings of control and experimental females were reared by unmanipulated, natural females in a uniform maternal environment; ii) a split-brood design that enabled us to assess the interaction between the mother's corticosterone treatment and that of the nestlings. 4. There were significant pre-natal effects of increased maternal corticosterone on nestling growth and survival. Offspring of females experiencing experimentally increased corticosterone were heavier and larger than offspring of control females. There also was a significant interaction between maternal corticosterone treatment and the corticosterone treatment to which young were exposed within the egg in their effect on nestling survival while in the nest; experimental young exhibited greater survival than control young, but only when reared by control mothers. There was also a significant effect of maternal corticosterone treatment on nestling stress reactivity and, in both experiments, on the eventual recruitment of offspring as breeding adults in the local population. 5. These patterns are broadly consistent with the environmental/maternal-matching hypothesis, and highlight the importance of disentangling pre- and post-natal effects of manipulations of maternal hormone levels on offspring phenotype.
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