Undefined
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB54823 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR9970960.fastq.gz | Fastqsanger.gz | |||
| ERR9970951.fastq.gz | Fastqsanger.gz | |||
| ERR9970952.fastq.gz | Fastqsanger.gz | |||
| ERR9970953.fastq.gz | Fastqsanger.gz | |||
| ERR9970954.fastq.gz | Fastqsanger.gz |
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Project description:Pregnancy-induced maternal microchimerism shapes neurodevelopment and behavior in mice
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Project description:Maternal obesity during pregnancy is associated with neurodevelopmental disorder (NDD) risk. We utilized integrative multi-omics to examine maternal obesity effects on offspring neurodevelopment in rhesus macaques by comparison to lean controls and two interventions. Differentially methylated regions (DMRs) from longitudinal maternal blood-derived cell-free fetal DNA (cffDNA) significantly overlapped with DMRs from infant brain. The DMRs were enriched for neurodevelopmental functions, methylation-sensitive developmental transcription factor motifs, and human NDD DMRs identified from brain and placenta. Brain and cffDNA methylation levels from a large region overlapping mir-663 correlated with maternal obesity, metabolic and immune markers, and infant behavior. A DUX4 hippocampal co-methylation network correlated with maternal obesity, infant behavior, infant hippocampal lipidomic and metabolomic profiles, and maternal blood measurements of DUX4 cffDNA methylation, cytokines, and metabolites. We conclude that in this model, maternal obesity was associated with changes in the infant brain and behavior, and these differences were detectable in pregnancy through integrative analyses of cffDNA methylation with immune and metabolic factors.
2022-08-23 | GSE171064 | GEO
Project description:“Dysbiosis" of the maternal gut microbiome, in response to environmental challenges such as infection, altered diet and stress during pregnancy, has been increasingly associated with abnormalities in offspring brain function and behavior. However, whether the maternal gut microbiome regulates neurodevelopment in the absence of environmental challenge remains unclear. In addition, whether the maternal microbiome exerts such influences during critical periods of embryonic brain development is poorly understood. Here we investigate how depletion, and selective reconstitution, of the maternal gut microbiome influences fetal neurodevelopment in mice. Embryos from antibiotic-treated and germ-free dams exhibit widespread transcriptomic alterations in the fetal brain relative to conventionally-colonized controls, with reduced expression of several genes involved in axonogenesis. In addition, embryos from microbiome-depleted mothers exhibit deficient thalamocortical axons and impaired thalamic axon outgrowth in response to cell-extrinsic guidance cues and growth factors. Consistent with the importance of fetal thalamocortical axonogenesis for shaping neural circuits for sensory processing, restricted depletion of the maternal microbiome from pre-conception through mid-gestation yields offspring that exhibit tactile hyposensitivity in select sensorimotor behavioral tasks. Gnotobiotic colonization of antibiotic-treated dams with a limited consortium of spore-forming bacteria indigenous to the gut microbiome prevents abnormalities in fetal brain gene expression, fetal thalamocortical axonogenesis and adult tactile sensory behavior associated with maternal microbiome depletion. Metabolomic profiling reveals that the maternal microbiota regulates levels of numerous small molecules in the maternal serum as well as the brains of fetal offspring. Select microbiota-dependent metabolites – trimethylamine N-oxide, 5-aminovalerate, imidazole propionate, and hippurate – sufficiently promote axon outgrowth from fetal thalamic explants. Moreover, maternal supplementation with the metabolites during early gestation abrogates deficiencies in fetal thalamocortical axons and prevents abnormalities in tactile sensory behavior in offspring from microbiome-depleted dams. Altogether, these findings reveal that the maternal gut microbiome promotes fetal thalamocortical axonogenesis and select tactile sensory behaviors in mice, likely by signaling of microbially modulated metabolites to neurons in the developing brain.
2020-04-17 | GSE147183 | GEO
Project description:Stress and glucocorticoid exposure during pregnancy alters neurodevelopment and behavior in offspring, and these effects extend multiple generations through a paternal lineage. The epigenetic mechanisms that govern this transgenerational transmission are unclear. We hypothesized that maternal exposure to multiple courses of sGC in late pregnancy would result in altered miRNA levels in germs cells of male guinea pigs across three generations. Further, our behavioral data indicate that F2 females exhibit altered behaviors following sGC exposure. Thus, we evaluated the miRNA profile of F2 female prefrontal cortex to determine the mechanisms responsible for these behavioral changes and to compare these data to our germ cell miRNA analysis. We used miRNA microarray to evaluate the miRNA levels in F1-F3 germ cells and F2 female PFC in guinea pigs that were exposed to control and F0 prenatal sGC exposure. We identified no significant changes to miRNA levels in both F1-F3 germ cells and F2 PFC from guinea pigs in the sGC group.
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Project description:Maternal overnutrition during pregnancy/or lactation predisposes offspring obesity and related metabolic syndromes in later life. Hypothalamus is the highest heterogeneous brain region located at the base of the brain that is critical to the regulation of the energy homeostasis.We investigated how the maternal programming shapes the single-nucleus transcriptomic landscapes in postnatal day15 offspring hypothalamus in a sex-specific manner.
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Project description:The microorganisms colonizing the gastrointestinal tract of animals, collectively referred to as the gut microbiome, affect numerous host behaviors dependent on the central nervous system (CNS). Studies comparing germ-free mice to normally colonized mice have demonstrated influences of the microbiome on anxiety-related behaviors, voluntary activity, and gene expression in the CNS. Additionally, there is epidemiologic evidence supporting an intergenerational influence of the maternal microbiome on neurodevelopment of offspring and behavior later in life. There is limited experimental evidence however directly linking the maternal microbiome to long-term neurodevelopmental outcomes, or knowledge regarding mechanisms responsible for such effects. Here we show that that the maternal microbiome has a dominant influence on several offspring phenotypes including anxiety-related behavior, voluntary activity, and body weight. Adverse outcomes in offspring were associated with features of the maternal microbiome including bile salt hydrolase (Bsh) expression, abundance of certain bile acids, and hepatic expression of S1pr2. In cross-foster experiments, offspring resembled their birth dam phenotypically, despite faithful colonization in the postnatal period with the surrogate dam microbiome. Genome-wide methylation analysis of hippocampal DNA identified microbiome-associated differences in methylation of 196 loci in total, 176 of which were imprinted by the maternal microbiome. Further, single-cell transcriptional analysis revealed accompanying differences in expression of several differentially methylated genes within certain hippocampal cell clusters, and vascular expression of genes associated with bile acid transport. Inferred cell-to-cell communication in the hippocampus based on coordinated ligand-receptor expression revealed differences in expression of neuropeptides associated with satiety. Collectively, these data provide proof-of-principle that the maternal gut microbiome has a dominant influence on the neurodevelopment underlying certain offspring behaviors and activities, and selectively affects genome methylation and gene expression in the offspring CNS in conjunction with that neurodevelopment.
2024-11-01 | GSE239371 | GEO
Project description:Numerous recent studies showed that early anesthesia during neurodevelopment may induce changes in specific behaviors. We further studied the effects of early anesthetic exposures regarding addiction behavior later in life. Postnatal day (PND) 16 C57BL/6 mice received ketamine anesthesia for 5 consecutive days. Addiction behavior was evaluated 1 week after anesthesia treatment. Neurological changes after repeated anesthesia were evaluated using high-performance liquid chromatography, RNA sequencing, electrophysiology studies. Repeated ketamine anesthesia during the critical neurodevelopment period increased the expression of genes involved with action potential, and induced excitatory/inhibitory (E/I) imbalance in hippocampal CA1 pyramidal neurons of male mice. Such neurological changes were associated with increases in drug-induced contextual addiction memory.
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Project description:Maternal prebiotic supplementation exacerbates colitis development in offspring mice
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Project description:During pregnancy, the energy requirements of the fetus impose changes in maternal metabolism. Increasing insulin resistance in the mother maintains nutrient flow to the growing fetus, while prolactin and placental lactogen counterbalance this resistance and prevent maternal hyperglycemia by driving expansion of the maternal population of insulin-producing beta-cells. However, the exact mechanisms by which the lactogenic hormones drive beta-cell expansion remain uncertain. Here we show that serotonin acts downstream of lactogen signaling to drive beta-cell proliferation. Serotonin synthetic enzyme Tph1 and serotonin production increased sharply in beta-cells during pregnancy or after treatment with lactogens in vitro. Inhibition of serotonin synthesis by dietary tryptophan restriction or Tph inhibition blocked beta-cell expansion and induced glucose intolerance in pregnant mice without affecting insulin sensitivity. Expression of the Gq-linked serotonin receptor Htr2b in maternal islets increased during pregnancy and normalized just prior to parturition, while expression of the Gi-linked receptor Htr1d increased at the end of pregnancy and postpartum. Blocking Htr2b signaling in pregnant mice also blocked beta-cell expansion and caused glucose intolerance. These studies reveal an integrated signaling pathway linking beta-cell mass to anticipated insulin need during pregnancy. Modulators of this pathway, including medications and diet, may affect the risk of gestational diabetes. Analysis of poly(A)+ RNA from 3 biological replicates of pancreatic islets isolated from normal female and pregnant female mice
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Project description:Maternal infections during pregnancy pose an increased risk for neurodevelopmental psychiatric disorders (NPDs) in the offspring. Here, we examined age- and sex-dependent dynamic changes of the hippocampal synaptic proteome after viral-like maternal immune activation (MIA) in embryonic and adult mice.
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