Effects of 2,3',4,4'5-Pentachlorobiphenyl Exposure during Pregnancy on Maturation of Offspring Oocytes in Mice
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE133488 | GEO | 2019/10/29
REPOSITORIES: GEO
Similar Datasets
Project description:Effects of 2,3',4,4'5-Pentachlorobiphenyl Exposure during Pregnancy on Maturation of Offspring Oocytes in Mice
| PRJNA551608 | ENA
Project description:Oocytes undergo a recently discovered mitochondrial proteome remodeling event in flies1, frogs1, and humans2. This oocyte mitochondrial remodeling event, which includes substantial changes in electron transport chain (ETC) subunit abundance1,2, is regulated by maternal insulin signaling1. However, why oocytes undergo mitochondrial remodeling is unknown, with some speculating that it might be a conserved mechanism to protect oocytes from genotoxic damage by reactive oxygen species (ROS)2. In Caenorhabditis elegans, we previously found that maternal exposure to osmotic stress drives a 50-fold increase in offspring survival in response to future osmotic stress, and that this intergenerational adaptation is regulated by insulin signaling to oocytes3. Here, we used proteomics and genetic manipulations to show that insulin signaling to oocytes regulates offspring’s ability to adapt to future stress via a mechanism that depends on ETC composition in maternal germ cells/oocytes. Specifically, we found that maternally expressed mutant alleles of nduf-7 (complex I subunit) or isp-1 (complex III subunit) altered offspring’s response to osmotic stress at hatching independently of offspring genotype. Furthermore, we found that expressing wild-type isp-1 in maternal germ cells (oocytes) was sufficient to restore offspring’s normal response to osmotic stress. Chemical mutagenesis screens revealed that oocyte ETC composition regulates offspring’s response to osmotic stress by altering AMP kinase function in offspring which in turn regulates both ATP and glycerol metabolism in offspring in response to continued osmotic stress. To our knowledge, these data are the first to show that changes in oocyte mitochondrial ETC composition can affect an animal phenotype that manifests after embryonic development is complete. The data also suggest that the reason diverse animals exhibit insulin regulated remodeling of oocyte mitochondria might be to tailor offspring metabolism to best match the environment of their mother.
2024-03-09 | GSE261225 | GEO
Project description:Oocyte composition can directly influence offspring fitness, particularly in oviparous species such as most insects, where it is the primary form of parental investment. Oocyte production is also energetically costly, dependent on female condition and responsive to external cues. We investigated whether mating influences mature oocyte composition in Drosophila melanogaster using a quantitative proteomic approach. Our analyses robustly identified 4,485 oocyte proteins and revealed that stage-14 oocytes from mated females differed significantly in protein composition relative to oocytes from unmated females. Proteins forming a highly interconnected network enriched for translational machinery and transmembrane proteins were increased in oocytes from mated females, including calcium binding and transport proteins. This mating-induced modulation of oocyte maturation was also significantly associated with proteome changes that are known to be triggered by egg activation. We propose that these compositional changes are likely to have fitness consequences and adaptive implications given the importance of oocyte composition, rather than active gene expression, to the maternal-to-zygotic transition and early embryogenesis.
2021-02-24 | PXD022142 | Pride
Project description:Bisphenol S (BPS) is widely used to replace earlier-eliminated BPA. We evaluated the effect of acute in vivo BPS exposure on oocyte quality using eight-weeks-old ICR female mice (N = 15 per experimental group), exposed to vehicle or BPS1-BPS4 (0.001, 0.1, 10, and 100 ng BPS x g bw-1 x day-1, respectively). Oocytes were isolated and matured in vitro. Thereafter, we observed that BPS exposure increases aberrant spindle formation in mature oocytes and induces DNA damage. Moreover, BPS3 significantly increases chromatin repressive marks 5-methyl cytosine (5meC) and H3K27me2 in immature oocytes. In the BPS2 group (0.1 ng x g bw-1 x day-1), the increase in 5meC arises during oocyte maturation. Transcriptome analysis shows differential expression of early embryonic development transcripts in BPS2-exposed oocytes. These findings indicate that the biological effect of BPS is non-monotonic, affecting oocyte quality even at concentrations that are orders of magnitude below those measured in humans. We used microarray aproach to unravel gene expression differences triggered by the administration of BPS at different concentrations in mouse oocytes.
2020-05-22 | GSE140640 | GEO
Project description:In order to establish an obese mouse model, female mice were continuously fed with a high-fat diet (HFD) or a normal diet (control) for 16 weeks beginning at three weeks of age. In this paper, these mice are termed ‘HFD mice’ and ‘control mice’, respectively. Accordingly, we call their oocytes ‘HFD oocytes’ and ‘control oocytes’. Substantial evidence indicates that the effects of maternal obesity on embryo/offspring development can be attributed to factors within the oocyte (9). To identify such potential effectors, we performed a comparative proteomic analysis of ovulated MII oocytes from control and HFD mice.
2018-05-24 | PXD006641 | Pride
Project description:Epigenetic modifications regulate transcriptional access to unique cell-type-specific gene sets, which define cell differentiation and tissue development. Cell-to-cell heritability of this information provides long-term molecular memories that define cell lineage identities. Germline epigenetic programming, including genomic imprinting, can substantially alter offspring development, but the mechanisms are poorly understood. In this study we demonstrate that the essential polycomb complex gene, Eed, regulates histone methylation in a large cohort of non-imprinted developmental genes in mouse and human oocytes. Using a model that facilitates the separation of genetic and epigenetic inheritance, we show that Eed establishes H3K27me3 during a unique widow of early oocyte growth and is essential in mouse oocytes for mediating a complex program that controls fetal growth and co-ordinated development of multiple tissues in late-stage fetal offspring, including bone, brain and placenta. Our study defines a new role for Eed in epigenetic inheritance that profoundly affects offspring growth and development.
2024-06-30 | GSE210397 | GEO
Project description:The success of human reproduction relies on high quality oocytes. Oocyte quality is manifested by the competence to complete meiosis, to be fertilized, and to support embryonic development. This meiotic and developmental competence is gradually established during the course of oocyte and follicle development, and is determined in large part by the autonomous gene expression program intrinsic to the oocyte. In order to explore the regulatory role of LSM14B in oocyte, we analyzed the effect of Lsm14b KO on gene expression in GV-stage fully-grown oocytes (FGOs) in mice by comparing the corresponding transcriptomes via RNA-Seq Analysis.
2023-09-08 | GSE204773 | GEO
Project description:Metabolic stress associated with negative energy balance in high producing dairy cattle and obesity in women is a risk factor for decreased fertility. Non-esterified fatty acids (NEFA) are involved in this pathogenesis as they jeopardize oocyte and embryo development. Growing evidence indicates that maternal metabolic disorders can disturb epigenetic programming, and more specifically DNA methylation, in the offspring. Final oocyte maturation and early embryo development coincide with specific methylation changes and both time periods are sensitive to adverse environments. Therefore, we investigated whether elevated NEFA concentrations affect the establishment and maintenance of DNA methylation patterns in oocytes and embryos and subsequently alter transcriptomic profiles and developmental competence of the resultant blastocysts. To do this, bovine oocytes and embryos were exposed to different NEFA concentrations in two separate experiments. In the first experiment, oocytes were matured in vitro for 24 hours in medium containing: 1) physiological (âBASALâ) concentrations of oleic (OA), palmitic (PA) and stearic (SA) or 2) elevated (pathophysiological or âHIGH COMBIâ) concentrations of OA, PA and SA. In the second experiment, zygotes were cultivated in vitro for 6.5 days under BASAL or HIGH COMBI conditions. The developmental competence was evaluated by assessing cleavage and blastocyst rate. Overall gene expression and DNA methylation of resultant blastocysts were analyzed using microarray techniques. Data regarding DNA methylation were re-evaluated by pyrosequencing. HIGH COMBI-exposed oocytes and embryos displayed a lower competence to develop into blastocysts compared to their BASAL-exposed counterparts (19.3 % compared to 23.2 % and 18.2 % compared to 25.3 %, respectively) (P < 0.05). HIGH COMBI-exposed oocytes and embryos resulted in blastocysts with altered DNA methylation profiles and transcriptomic fingerprints, compared to BASAL-exposed counterparts. Differences in gene expression and methylation were more pronounced after exposure during culture compared to maturation suggesting that zygotes are more susceptible to an adverse environment. Main gene networks affected were related to lipid and carbohydrate metabolism, cell death, immune response and metabolic disorders. This may offer clues regarding the high rate of embryonic loss and metabolic diseases during later stages of life observed in offspring from mothers displaying lipolytic disorders. Two experiments were set up to characterize the epigenomic profile of the resultant day 7.5 blastocysts. In the first (in vitro maturation or IVM) experiment, the effect of elevated NEFA exposure during oocyte maturation (24 h) on DNA methylation profiles was evaluated by exposing oocytes to the BASAL or HIGH COMBI conditions. In the second (in vitro culture or IVC) experiment, the effect of elevated NEFA exposure during embryo culture (6.5 days) on DNA methylation marks was evaluated by exposing embryos to the BASAL or HIGH COMBI conditions. A total of 1039 and 1412 oocytes were used in the IVM and IVC experiment, respectively, equally distributed between treatments in 4 replicates. Resultant day 7.5 blastocysts were snap frozen for subsequent DNA methylation analysis (80 blastocysts in each experiments, equally collected between treatments in 4 replicates).
2016-06-28 | E-GEOD-83766 | biostudies-arrayexpress
Project description:To investigate how exposure to morphine during the prenatal and early postnatal period affects the offspring prefrontal cortex in a mouse model We performed gene expression profiling analysis using data obtained from RNA-seq of offspring prefrontal cortical brain samples at postnatal day 21
2022-10-26 | GSE206032 | GEO
Project description:Autism spectrum disorder (ASD) is a highly heterogeneous neurodevelopmental disorder that significantly jeopardizes the physical and mental well-being of children. Autism spectrum disorder results from a combination of environmental and genetic factors. Hyperandrogenic exposure during pregnancy increases their risk of developing autism. Nevertheless, the prenatal exposure to androgens affects offspring neurodevelopment and the underlying mechanisms have not been fully elucidated. In the present study, administration of excessive dihydrotestosterone (DHT) to pregnant mice was found to impair neuronal development and dendritic spine formation in offspring, inducing autism-like behaviors. Furthermore, through mRNA transcriptome sequencing technology, the key molecule Nr4a2 was identified during this process of change. Overexpression of Nr4a2 and treatment with amodiaquine (AQ) significantly improved the abnormal phenotypes in offspring caused by prenatal exposure to androgens. Overall, Nr4a2 emerges as a crucial molecule involved in the impairment of offspring neurodevelopment due to prenatal androgen exposure, which provides a new perspective for the in-depth study of the influencing factors and underlying mechanisms.
2023-11-04 | GSE246534 | GEO