Effects of maternal Cd on the female reproductive functions, gametes development and genes expression of zebrafish
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ABSTRACT:
ORGANISM(S): Danio rerio
PROVIDER: GSE20926 | GEO | 2013/07/01
SECONDARY ACCESSION(S): PRJNA124363
REPOSITORIES: GEO
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Project description:The impacts of maternal Cd on zebrafish from female to embryo which included fecundity, gametes development, growth, other reproductive functions, and gene expression of 5hpf embryo were up and down regulated after female pretreated with Cd. The mating rate decreased by 30 %. It can be observed in growth delay during 6-somite stage. The ceratohyal head angle of larvae is widest upon 35.6 M-NM-<M maternal Cd treatment and it was showed a dose response. Besides, pericardial edema occurred in some 96hpf larvae. There were showed 33 and 37 target genes appeared significantly down and up regulation after microarray assay, respectively. The major effect on gene up regulation was showed at the functional of transcription (occupied 18.9%) and down regulation at the functional of protein biosynthesis (occupied 33.3%). These results demonstrated that maternal Cd influenced the reproduction ability of female and causes development abnormal of embryo. Sexually mature zebrafish (D. rerio) of both sexes, obtained from the Institute of Cellular and Organismic Biology, Academia Sinica (Taipei, Taiwan), were kept in an aquarium supplied with dechlorinated, circulated, aerated local tap water at 28 M-BM-0C with a 14: 10-h light/dark cycle, and were fed Daphnia and shrimp. Fertilized eggs were incubated in M-bM-^@M-^\zebrafish solutionM-bM-^@M-^\ (E3 solution) which contained 5 mM NaCl, 0.17 mM KCl, 0.33 mM CaCl2, 0.33 mM MgSO4, and 1 ppm methylene blue (pH 7.2). Developing embryos of 5 h post-fertilization (hpf) were collected for total RNA extraction, and process of microarray assay. The number of hatched zebrafish larvae at 48 and 72 hpf were recorded. The larvae of 72 hpf larvae were collected for cartilage stain in order to observe the development of pharyngeal arch. Nguyen and Janssen (2001) reported that the LC50 at 96 h of Cd was 0.62~1.33 M-NM-<M for 12-dpf stage zebrafish, and our previous study showed that the zebrafish embryo could induced physiological response with 0.89 M-NM-<M Cd exposure (Wu et al., 2008). Hence, a 10M-CM-^W (8.9 M-NM-<M) , 20M-CM-^W (17.8 M-NM-<M) and 40M-CM-^W (35.6 M-NM-<M) dose of 0.89 M-NM-<M was used in female zebrafish. The Cd medium was prepared using completely dried CdCl2 (Sigma, St. Louis, MO) dissolved in 1 mL concentrated HCl; double-deionized water was used to prepare the 10 mg/L Cd stock solution, which was then diluted with zebrafish solution before being used in the exposure experiments. During all experiments, the test containers were cleaned with HNO3 and thoroughly rinsed with double-deionized water before use.
2013-07-01 | E-GEOD-20926 | biostudies-arrayexpress
Project description:Cadmium (Cd) administered to female C57BL/6 mice on gestation day 8 induces a high incidence of anterior neural tube defects (exencephaly). This adverse effect can be attenuated by maternal pretreatment with zinc (Zn). In this study we used replicated microarray analysis to investigate gene expression changes induced in the embryo 5 h after maternal Cd exposure in the absence or presence of Zn pretreatment.
2006-04-11 | E-MEXP-529 | biostudies-arrayexpress
Project description:After fertilization the developing mammalian embryo migrates through the oviduct before it implants in the uterus. In order to prevent tubal pregnancy or failed implantation, development and migration of the embryo has to be tightly coordinated1. The precise molecular basis for the regulation of this maternal-embryonic interaction is largely unknown. Here we show that the Wilms tumor suppressor protein Wt1 is a critical regulator of the interaction between the maternal environment and the early embryo. Our results indicate that subfertility in Wt1ko/+ females is a maternal effect caused by the Wt1-dependent de-regulation of Prss29, encoding a serine protease. Notably, blocking Prss29 activity was sufficient to rescue subfertility in Wt1ko/+ female mice indicating Prss29 as a critical factor in female fertility. Furthermore, we have identified a missense mutation in a patient with idiopathic infertility leading to an amino acid exchange within the zinc finger domain of WT1 and resulting in reduced DNA binding. We demonstrate that Wt1 represses expression of Prss29 and that its de-repression and precocious expression in the oviduct interferes with pre-implantation development. Our study reveals a novel role for Wt1 in early mammalian development and identifies proteases as critical mediators of the maternal-embryonic crosstalk. We believe that our data regarding the importance of a proteostatic environment in the oviduct are also relevant for female fertility in humans. We anticipate that our findings will form the basis for the identification of further causes of idiopathic infertility.
2017-04-04 | PXD003283 | Pride
Project description:Phytoremediation soil polluted by heavy metal has been drawn on a worldwide attention from human society. However, how to improve the efficiency of plant remediation of soil contaminated by cadmium remains unknown. Previous studies showed that nitrogen (N) significantly enhanced cadmium uptake in poplar plants. In order to further explore the key role of N in the detoxification against cadmium stress in plants, this study try to investigate the poplar proteome and phosphoproteome difference between Cd stress and Cd+N treatment. In total, 5838 of the 6573 identified were quantified. With a fold-change threshold >1.3 and p-value<0.05, 375 and 108 proteins were up- and down-regulated by Cd stress when compared to the control, 42 and 89 proteins were up- and down-regulated, respectively, in Cd+N / Cd group, 522 and 127 proteins were up- and down-regulated, respectively, in Cd+N / CK group. In addition, the phosphoproteome data was obtained after the proteomic difference was normalized, and 1471phosphosites in 721 proteins were quantified. Based on a fold-change threshold >1.2, P-value <0.05, the Cd stress up-regulated 8 phosphosites in 8 proteins and down-regulated 69 phosphosites in 58 proteins, whereas N+Cd treatment up-regulated 95 phosphosites in 86 proteins and down-regulated 17 phosphosites in 17 proteins when compared to sole Cd stress. In addition, N+Cd treatment up-regulated 74 phosphosites in 60 proteins and down-regulated 42 phosphosites in 37 proteins when compared to the control.Several putative responses to stress proteins, transcriptional and translational regulation factors were up-regulated by addition ofexogenous nitrogen followed Cd stress at the proteome and phosphoproteome levels. Especially, heat shock protein 70 (HSP70), peroxidase (POD), zinc finger protein (ZFP), ABC transporter protein (ABC), eukaryotic translation initiation factor (elF) and splicing factor 3B subunit 1-like (SF3BI) were up-regulated by Cd+N treatment whether at the proteome or at the phosphoproteome levels, which was need to further study. In a word, taken together of proteome and phosphoproteome data, nitrogen serves a protective role in plants treated with Cd by multiple ways.
2020-05-26 | PXD013360 | Pride
Project description:Egg cells represent the female partner that fuses with the sperm cell during fertilization in all multi-cellular eukaryotic organisms—and, in flowering plants, is a founder of the embryo. We examined the transcriptome of Oryza sativa ssp. japonica (cv Katy) using the Affymetrix 57K rice genome GeneChip to provide an overview of genes activated in the maternal gamete, transcripts transmitted by the paternal genome, and changes in transcript up- and down-regulation during fertilization. We used microarrays to detail the global program of gene expression in the egg cell at anthesis, complementing prior data on the male germ lineage, and following gene expression during fertilization and gamete fusion.
2022-12-31 | GSE27400 | GEO
Project description:This study aimed to assess PFAS distribution and lung proteome changes in CD-1 offspring after gestational and lactational exposure to PFOS, PFOA, PFHxS, or a PFAS mix. A secondary aim was to evaluate how maternal exposure to a high fat diet (HFD) affected the latter endpoints. Pregnant CD-1 mice received PFOA, PFOS, PFHxS (1 mg/kg), a PFAS mix (1 mg/kg each), or vehicle. Dams were fed standard diet (SD) or high fat diet (HFD), and PFAS were administered from gestation day 1 to postnatal day 20. At PND 21, lung PFAS concentration was measured using LC-MS/MS, and proteomic analysis was conducted. Results from LC-MS/MS analysis showed a significant overall difference in PFOS, PFOA, and PFHxS levels and the treatment groups with PFHxS concentration were significantly higher compared to PFOS and PFOA. Proteomic analysis determined female pups exposed to maternal HFD Mix (Mix HFD female) and PFOS (PFOS HFD female) had the most differentially expressed proteins followed by PFOS SD male, Mix SD female, and Mix SD male. Canonical pathways like EIF2 signaling, mTOR signaling, and mitochondrial dysfunction were differentially modulated. This study provides insights into PFAS distribution, the molecular mechanism, biomarkers on the neonatal lung in animal models following perinatal exposure.
2023-12-06 | MSV000093587 | MassIVE
Project description:In zebrafish, vitellogenic oocytes can incorporate significant amounts of 17β-estradiol released from nearby granulosa cells according to a first-order kinetics, since the steroid low polarity ensures high permeability and affinity for yolk lipids. Estrogen bioactivity is likely, because the maternal mRNA for the estrogen receptor-β2 (ers2a) is highly expressed in ovulated oocytes. This transcript is available for translation in the embryo until its sharp decline from 4 to 8 hours post-fertilization (hpf), being replaced by low levels of zygotic ers2a mRNA from 24 hpf to hatching at 48 hpf, as determined by qRT-PCR. Estrogen receptors-α and -β1 are only expressed zygotically at low levels from 24 hpf onwards. To test the functional role of maternal ers2a mRNA, 1- or 2-cell embryos were injected with 10.3 ng each of morpholino to knockdown translation (MO2-ers2a) of both maternal and zygotic ers2a transcripts, missplicing morpholino (MO3-ers2a) to block post-transcriptionally the zygotic transcript alone, and a nonspecific morpholino (MO-control) as a control. Treatment with MO2-ers2a caused severe malformations in 63% of 1-5 dpf larvae, as compared to 10-11% in those treated with MO3-ers2a and MO2-control. Defects included body growth delay and curved shape, abnormal brain and splanchnocranium development, enlarged and hemorrhagic pericardial cavity, uninflated swim bladder and rudimentary caudal fin with aberrant circular motion. Affected larvae could survive for only 12-14 days. Co-injection of an anti-p53 MO failed to rescue the MO2-ers2a-phenotypes, eliminating the possibility of off-target effects. Pangenomic microarray analysis revealed that 240 and 219 significantly expressed transcripts were up- and down-regulated, respectively, by maternal Ers2a protein deficiency in 8-hpf MO2-ers2a-embryos. Also at 48 hpf, 162 and 120 presumably zygotic transcripts were up- and down-regulated, respectively, but only 18 were in common with each of the 8-hpf sets. Whole-mount in situ hybridization revealed an intensified expression of the genes six3.1 and emx1 in MO2-ers2a-embryos at 24-48 hpf, as compared to controls. These findings suggest the involvement of maternal ers2a mRNA in the epigenetic programming of zebrafish development. MO2-ers2a morphants were compared with MO-control at 8 hpf and 48 hpf. MO2-ers2a is a morpholinos selected to knockdown translation of ers2a mRNA
2011-01-12 | E-GEOD-24934 | biostudies-arrayexpress
Project description:Maternal inactivation of genes encoding components of the sub-cortical maternal complex (SCMC) and its associated member PADI6 generally results in early embryo lethality. In humans, SCMC gene variants were found in the healthy mothers of children affected by multi-locus imprinting disturbances (MLID). However, how the SCMC controls the DNA methylation required to regulate imprinting remains poorly defined. We generated a mouse line carrying a Padi6 missense variant that was identified in a family with Beckwith-Wiedemann syndrome and MLID. If homozygous in female mice this variant resulted in interruption of embryo development at the 2-cell stage. Single-cell multi-omic analyses demonstrated defective maturation of Padi6-mutant oocytes and incomplete DNA demethylation, down-regulation of zygotic genome activation (ZGA) genes, up-regulation of maternal decay genes and developmental delay in 2-cell embryos developing from Padi6-mutant oocytes, but little effect on genomic imprinting. Western blotting and immunofluorescence analyses showed reduced level of UHRF1 in oocytes and abnormal localization of DNMT1 and UHRF1 in both oocytes and zygotes. Treatment with 5-azacytidine reverted DNA hypermethylation but did not rescue the developmental arrest of mutant embryos. Taken together, this study demonstrates that PADI6 controls both nuclear and cytoplasmic oocyte processes that are necessary for pre-implantation epigenetic reprogramming and ZGA.
2023-10-18 | GSE245424 | GEO
Project description:Maternal inactivation of genes encoding components of the sub-cortical maternal complex (SCMC) and its associated member PADI6 generally results in early embryo lethality. In humans, SCMC gene variants were found in the healthy mothers of children affected by multi-locus imprinting disturbances (MLID). However, how the SCMC controls the DNA methylation required to regulate imprinting remains poorly defined. We generated a mouse line carrying a Padi6 missense variant that was identified in a family with Beckwith-Wiedemann syndrome and MLID. If homozygous in female mice this variant resulted in interruption of embryo development at the 2-cell stage. Single-cell multi-omic analyses demonstrated defective maturation of Padi6-mutant oocytes and incomplete DNA demethylation, down-regulation of zygotic genome activation (ZGA) genes, up-regulation of maternal decay genes and developmental delay in 2-cell embryos developing from Padi6-mutant oocytes, but little effect on genomic imprinting. Western blotting and immunofluorescence analyses showed reduced level of UHRF1 in oocytes and abnormal localization of DNMT1 and UHRF1 in both oocytes and zygotes. Treatment with 5-azacytidine reverted DNA hypermethylation but did not rescue the developmental arrest of mutant embryos. Taken together, this study demonstrates that PADI6 controls both nuclear and cytoplasmic oocyte processes that are necessary for pre-implantation epigenetic reprogramming and ZGA.
2023-10-18 | GSE245423 | GEO
Project description:Maternal inactivation of genes encoding components of the sub-cortical maternal complex (SCMC) and its associated member PADI6 generally results in early embryo lethality. In humans, SCMC gene variants were found in the healthy mothers of children affected by multi-locus imprinting disturbances (MLID). However, how the SCMC controls the DNA methylation required to regulate imprinting remains poorly defined. We generated a mouse line carrying a Padi6 missense variant that was identified in a family with Beckwith-Wiedemann syndrome and MLID. If homozygous in female mice this variant resulted in interruption of embryo development at the 2-cell stage. Single-cell multi-omic analyses demonstrated defective maturation of Padi6-mutant oocytes and incomplete DNA demethylation, down-regulation of zygotic genome activation (ZGA) genes, up-regulation of maternal decay genes and developmental delay in 2-cell embryos developing from Padi6-mutant oocytes, but little effect on genomic imprinting. Western blotting and immunofluorescence analyses showed reduced level of UHRF1 in oocytes and abnormal localization of DNMT1 and UHRF1 in both oocytes and zygotes. Treatment with 5-azacytidine reverted DNA hypermethylation but did not rescue the developmental arrest of mutant embryos. Taken together, this study demonstrates that PADI6 controls both nuclear and cytoplasmic oocyte processes that are necessary for pre-implantation epigenetic reprogramming and ZGA.
2023-10-18 | GSE245425 | GEO