Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

14 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptional consequences of Zfy1 and Zfy2 expression in GV oocytes

ABSTRACT: Sex-reversed ‘XYSry-’ female mice that lack Sry due to the 11 kb deletion Srydl1Rlb have very limited fertility, partly due to the effects of posessing only a single X chromosome. However, the fertility deficit is even worse in sex-reversed XY females than in XO females, implicating Y-linked genes in the further loss of fertility. Transgenic addition of Yp-linked genes to XO females and also to normal XX females implicated Zfy2 (but not the related Zfy1) as the cause of this effect. This study examines the transcriptional effects of Zfy2 and Zfy1 in GV oocytes from normal XX females. 18 samples representing 3 biological replicates from each of 6 genotypes. Genotypes are XX (normal control); XX,Zfy2-nf (control with non-functional Zfy2 transgene); XX,Zfy2 (with Zfy2 transgene); XX,Zfy2+Eif2s3y (contaminated sample, XX with Zfy2 transgene and also an Eif2s3y transgene in proportion of the cells), XX,Zfy1-lo (with single-copy Zfy1 transgene); XX-Zfy1-hi (with multi-copy Zfy1 transgene).

ORGANISM(S): Mus musculus

SUBMITTER: Peter Ellis

PROVIDER: E-GEOD-52218 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

The presence of the Y-chromosome, not the absence of the second X-chromosome, alters the mRNA levels stored in the fully grown XY mouse oocyte

Project description:The oocytes of B6.Y(TIR) sex-reversed female mouse mature in culture but fail to develop after fertilization because of their cytoplasmic defects. To identify the defective components, we compared the gene expression profiles between the fully-grown oocytes of B6.Y(TIR) (XY) females and those of their XX littermates by cDNA microarray. 173 genes were found to be higher and 485 genes were lower in XY oocytes than in XX oocytes by at least 2-fold. We compared the transcript levels of selected genes by RT-PCR in XY and XX oocytes, as well as in XO oocytes missing paternal X-chromosomes. All genes tested showed comparable transcript levels between XX and XO oocytes, indicating that mRNA accumulation is well adjusted in XO oocytes. By contrast, in addition to Y-encoded genes, many genes showed significantly different transcript levels in XY oocytes. We speculate that the presence of the Y-chromosome, rather than the absence of the second X-chromosome, caused dramatic changes in the gene expression profile in the XY fully-grown oocyte. We compared the gene expression profiles between the fully-grown oocytes of B6.Y(TIR) (XY) females and those of their XX littermates by cDNA microarray Mouse GV oocytes of B6.Y(TIR) were collected for RNA extraction and hybridization to Affymetrix microarray. We sought to extract the differentially expressed genes in the XY oocytes.

2013-04-02 | E-GEOD-45668 | biostudies-arrayexpress

Transcriptional consequences of Zfy1 and Zfy2 expression in GV oocytes

Project description:Sex-reversed ‘XYSry-’ female mice that lack Sry due to the 11 kb deletion Srydl1Rlb have very limited fertility, partly due to the effects of posessing only a single X chromosome. However, the fertility deficit is even worse in sex-reversed XY females than in XO females, implicating Y-linked genes in the further loss of fertility. Transgenic addition of Yp-linked genes to XO females and also to normal XX females implicated Zfy2 (but not the related Zfy1) as the cause of this effect. This study examines the transcriptional effects of Zfy2 and Zfy1 in GV oocytes from normal XX females.

2013-11-27 | GSE52218 | GEO

Growth hormone supplementation reduces aneuploidy and improves the quality of oocytes by activating ERK1/2 pathway in aged mice

Project description:The decline in oocyte quality is a limiting factor of female fertility; however, strategies to maintain the oocyte quality of aged women are not available. In this study, we showed that growth hormone (GH) supplementation in vivo not only alleviated the decline in oocyte number caused by aging, but also improved the quality and developmental potential of aged oocytes. Strikingly, GH supplementation reduced aneuploidy in aged oocytes. Proteomic analysis indicated that the ERK1/2 pathway was involved in the reduction in aneuploidy rate of aged oocytes, as confirmed both in vivo and in vitro. In addition, JAK2 might be involved in the regulation of ERK1/2 by GH in aged oocytes. Collectively, our findings revealed that GH supplementation protects oocytes from aging-related aneuploidy and enhances the quality of aged oocytes, and could be used to improve the outcome of assisted reproduction in aged women.

2023-07-20 | PXD039147 | Pride

Quantitative proteomic analysis of oocytes from high-fat diet (HFD)-fed and normal diet mice

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

Cordycepin Delays Postovulatory Aging of Mammalian Oocytes through Inhibition of Maternal mRNAs Degradation via DCP1A Polyadenylation Suppression

Project description:Postovulatory aging leads to the decline in oocyte quality and subsequent impairment of embryonic development, thereby reducing the success rates of assisted reproductive technology (ART). Nevertheless, potential preventative strategies to improve aging oocytes quality and the associated underlying mechanisms warrant further investigation. In this study, we identify cordycepin, an natural nucleoside analogue, as having the potential to restore the postovulatory aging-induced decline in oocyte quality, including aspects such as oocyte fragmentation, embryonic developmental competence, spindle/chromosomes morphology and mitochondrial function. Proteomic and RNA sequencing analyses revealed that cordycepin inhibited the degradation of several crucial maternal proteins and mRNAs caused by aging. Mechanistically, cordycepin was found to suppress the elevation of DCP1A protein levels by inhibiting polyadenylation during postovulatory aging, consequently impeding the decapping of maternal mRNAs. In humans, the increased degradation of DCP1A and total mRNA during aging was also inhibited by cordycepin. Collectively, our findings demonstrate that cordycepin may prevent postovulatory aging of mammalian oocytes by inhibition of maternal mRNAs degradation via DCP1A polyadenylation suppression, thereby promoting the successful rates of ART procedure.

2024-01-26 | PXD042600 | Pride

Microarray data of prepubertal, peripubertal, and adult oocytes, and from GV and MII oocytes matured in vivo or in vitro

Project description:Expression data from prepubertal, peripubertal, and adult derived mouse oocytes, and from germinal vesicle (GV), in vivo matured, and in vitro matured mouse oocytes. Oocytes derived from prepubertal females, or oocytes matured in vitro, are less developmentally competent compared to adult derived, or in vivo matured, oocytes, indicated by decreased embryonic development. One potential mechanism for decreased developmental potetential in prepubertal or in vitro matured oocytes is inadequate or inappropriate RNA degradation during oocyte maturation (progression from GV to MII). To investigate mechanisms involved in establishing oocyte cytoplasmic maturation and developmental competence, Affymetrix GeneChip microarrays were used. Keywords: Oocyte developmental competence The study encompassed three experimental designs using female B6D2F1 mice: 1) In vitro matured oocytes were obtained from d20 (prepubertal), d26 (peripubertal), and 7-8 wk old (adult) mice; 2) in vivo and in vitro matured oocytes were obtained from d26 mice; and 3) GV, in vivo matured, and in vitro matured oocytes were obtained from 7-8 wk old mice. RNA was extracted from pools of 150 oocytes and hybridized onto the Affymetrix microarrays.

2010-07-12 | E-GEOD-12432 | biostudies-arrayexpress

Transcription profiling of Mus musculus, Bos taurus, Xenopus laevis oocytes

Project description:Identification of genes expressed in oocytes and conserved in three different species with a multi-species cDNA microarray.

2006-01-31 | E-MEXP-488 | biostudies-arrayexpress

Transcription profiling of immature germinal vesicle stage oocytes with mature metaphase II oocytes to identify and characterize the changed and stable transcripts during mouse oocyte maturation.

Project description:There is massive destruction of transcripts during maturation of mouse oocytes. The objective of this project was to identify and characterize the transcripts that are degraded versus those that are stable during the transcriptionally silent germinal vesicle (GV)-stage to metaphase II (MII)-stage transition using the microarray approach. A system for oocyte transcript amplification using both internal and 3'-poly(A) priming was utilized to minimize the impact of complex variations in transcript polyadenylation prevalent during this transition. Transcripts were identified and quantified using Affymetrix Mouse Genome 430 v2.0 GeneChip. The significantly changed and stable transcripts were analyzed using Ingenuity Pathways Analysis and GenMAPP/MAPPFinder to characterize the biological themes underlying global changes in oocyte transcripts during maturation. It was concluded that the destruction of transcripts during the GV to MII transition is a selective rather than promiscuous process in mouse oocytes. In general, transcripts involved in processes that are associated with meiotic arrest at the GV-stage and the progression of oocyte maturation, such as oxidative phosphorylation, energy production, and protein synthesis and metabolism, were dramatically degraded. In contrast, transcripts encoding participants in signaling pathways essential for maintaining the unique characteristics of the MII-arrested oocyte, such as those involved in protein kinase pathways, were the most prominent among those stables. Experiment Overall Design: Comparison immature GV-stage oocyte (3 biological replicates) with mature MII-stage oocytes (3 biological replicates)

2007-11-13 | E-GEOD-5668 | biostudies-arrayexpress

Transcription profiling of mouse in vivo matured MII oocytes and fully in vivo grown germinal vesicle oocytes to identify gene transcripts linked to epigenetic reprogramming

Project description:To elucidate some of the tools involved in early embryonic reprogramming, the levels of gene transcripts believed to be of importance to epigenetic modifications, and chromatin remodeling were detected by oligonucleotide microarrays in in vivo matured MII oocytes and compared with fully in vivo grown GV oocytes.

2007-07-02 | E-MEXP-1146 | biostudies-arrayexpress

Transcription profiling of mouse, bovine and xenopus germinal vesicle stage oocytes reveals a high degree of conservation among species

Project description:Comparative analysis of bovine, mouse and xenopus oocyte transcript profiles. The results from bovine and xenopus germinal vesicle stage oocytes in this experiment were compared to previously-published microarray data on preimplantation development in the mouse (Carter 2003).

2008-02-01 | E-MEXP-1339 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data