Comparing the Transcriptomes of Wild Type and Mtor-Gdf9-Cre mediated Oocyte-Conditional Knockout Mouse ovaries by RNA-Seq Analysis
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE98497 | GEO | 2018/06/01
REPOSITORIES: GEO
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Project description:The goal of this study is to identify the differentially expressed genes in Gdf9-Cre and Zp3-Cre mediated Mtor oocyte-specific knockout (CKO) GV-stage fully-grown oocytes (FGO) by comparing their transcriptomes with that of the wild-type (WT) via RNA-Seq Analysis.
2018-06-01 | GSE114126 | GEO
Project description:Purpose: The goal of this study is to compare oocyte transcriptome profiling in WT and Kat8 Gdf9 cKO mice Methods: Oocyte mRNA profiles of 2 weeks old WT and Kat8 Gdf9 cKO mice were generated by deep sequencing using Illumina HiSeq 2500. Results: Using an optimized data analysis workflow, we mapped about 54-63 million sequence reads per sample to the mouse genome (build mm10) and identified 18,468 transcripts in the oocytes of WT and Kat8 Gdf9 cKO mice. Approximately 5% of the transcripts showed differential expression between the WT and Kat8 Gdf9 cKO oocyte, with a fold change ≥1.5 and p value <0.05. Conclusions: Our study represents the first detailed analysis of oocyte transcriptomes after kat8 deletion, which is generated by RNA-seq technology.Our results show that Kat8 affects numerous gene expression in mouse oocytes.
2017-03-25 | GSE97026 | GEO
Project description:The goal of this study is to identify the differentially expressed genes in Zp3-Cre mediated Mtor oocyte-specific knockout (CKO) Metaphase II (MII) oocytes by comparing the transcriptomes of Wild-Type (WT) and CKO Mouse MII oocytes via RNA-Seq Analysis. Methods: mRNA profiles of 3 sets of super-ovulated MII oocytes collected from 24-day old WT- and Mtor CKO female mice were generated by deep sequencing using an Illumina Hiseq2500 platform with 41bp single read. All RNA-seq reads passed filter were trimmed to remove low-quality bases and adaptor sequences. Reads then were aligned to the mm10 reference genome using tophat2 (v2.0.8b). Reads aligned to genes are counted by cufflinks (v2.1.1). The FPKMs are normalized usingcuffnorm. Differentially expressed genes are calculated using cuffdiff.
2021-05-01 | GSE98548 | GEO
Project description:EXOSC10 is a catalytic subunit of the nuclear RNA exosome with an exoribonuclease activity. The enzyme processes and degrades different classes of RNAs. To delineate the role of EXOSC10 during oocyte growth, specific Exosc10 inactivation was performed in the oocytes from the primordial follicle stage onward using the Gdf9-iCre; Exosc10f/- mouse model (Exosc10cKO(Gdf9)). Exosc10cKO(Gdf9) female mice are infertile. The onset of puberty and the estrus cycle in mutants are initially normal and ovaries contain all follicle classes. By the age of eight weeks, vaginal smears reveal irregular estrus cycles and mutant ovaries display a complete depletion of follicles. Mutant oocytes retrieved from the oviduct are degenerated, sometimes showing an enlarged polar body which may reflect a defective first meiotic division. Under fertilization conditions, the mutant oocytes do not enter into an embryonic development process. Furthermore, we conducted a comparative proteome analysis of wild type and Exosc10 knockout mouse ovaries and identified EXOSC10-dependent proteins involved in many biological processes, such as meiotic cell cycle progression and oocyte maturation. Our results unambiguously demonstrate an essential role for EXOSC10 in oogenesis and may serve as a model for primary ovarian insufficiency in humans.
2023-05-10 | PXD039417 | Pride
Project description:Gonadotropin-releasing hormone (GnRH) is secreted in brief pulses from the hypothalamus. GnRH regulates follicle-stimulating hormone b-subunit (FSHb) gene expression in pituitary gonadotropes in a frequency-sensitive manner that is central to reproductive physiology. The mechanisms underlying the preferential and paradoxical induction of FSHb by low frequency GnRH pulses are incompletely understood. Here, we identify growth differentiation factor 9 (GDF9) as a novel autocrine inducer of FSHb gene expression. GDF9 gene expression was preferentially suppressed by high frequency GnRH pulses due to reduced transcription. Exogenous GDF9 induced FSHb mRNA expression and knockdown or immunoneutralization of GDF9 reduced FSHb gene expression. Treatment with GDF9 stimulated Smad2/3 phosphorylation. The activin receptor-like kinase (ALK) receptor inhibitor SB-505124 antagonized GDF9-induced Smad2/3 phosphorylation and FSHb mRNA induction. Smad2 and Smad3 knockdown studies indicated that the induction of FSHb by GDF9 involves both Smad2 and Smad3. GDF9 and GnRH synergistically induced FSHb mRNA expression and high frequency GnRH pulses suppressed GDF9. We hypothesized that GDF9 contributes to a regulatory loop that tunes the GnRH frequency-response characteristics of the FSHb gene. To test this, we determined the effects of GDF9 knockdown on FSHb induction at different GnRH pulse frequencies using a parallel perifusion system. Reduction of GDF9 shifted the characteristic pattern of GnRH pulse frequency sensitivity. These results identify GDF9 as contributing to an incoherent feed-forward loop, comprised of both intracellular and secreted elementscomponents, that regulates FSHb expression in response to activation of the cell surface GnRH receptor. LbT2 microarray datasets as well as RNA-Seq data (GSE42120) were interrogated to determine the levels of expression of ALK4/5/7. LM-NM-2T2 cells were transfected with either scrambled siRNA or Gas siRNA for 48 h. RNA samples were snap-frozen in dry ice prior to whole-genome expression profiling analysis using MouseWG-6 v2.0 Expression BeadChip (Illumina, San Diego, CA). A total of 6 concentrated conditioned media samples were independently prepared: 3 replicates from control siRNA-treated cells, and 3 replicates from Gas siRNA-treated cells. This submission represents the microarray component of study.
2013-11-22 | E-GEOD-52631 | biostudies-arrayexpress
Project description:Gonadotropin-releasing hormone (GnRH) is secreted in brief pulses from the hypothalamus. GnRH regulates follicle-stimulating hormone b-subunit (FSHb) gene expression in pituitary gonadotropes in a frequency-sensitive manner that is central to reproductive physiology. The mechanisms underlying the preferential and paradoxical induction of FSHb by low frequency GnRH pulses are incompletely understood. Here, we identify growth differentiation factor 9 (GDF9) as a novel autocrine inducer of FSHb gene expression. GDF9 gene expression was preferentially suppressed by high frequency GnRH pulses due to reduced transcription. Exogenous GDF9 induced FSHb mRNA expression and knockdown or immunoneutralization of GDF9 reduced FSHb gene expression. Treatment with GDF9 stimulated Smad2/3 phosphorylation. The activin receptor-like kinase (ALK) receptor inhibitor SB-505124 antagonized GDF9-induced Smad2/3 phosphorylation and FSHb mRNA induction. Smad2 and Smad3 knockdown studies indicated that the induction of FSHb by GDF9 involves both Smad2 and Smad3. GDF9 and GnRH synergistically induced FSHb mRNA expression and high frequency GnRH pulses suppressed GDF9. We hypothesized that GDF9 contributes to a regulatory loop that tunes the GnRH frequency-response characteristics of the FSHb gene. To test this, we determined the effects of GDF9 knockdown on FSHb induction at different GnRH pulse frequencies using a parallel perifusion system. Reduction of GDF9 shifted the characteristic pattern of GnRH pulse frequency sensitivity. These results identify GDF9 as contributing to an incoherent feed-forward loop, comprised of both intracellular and secreted elementscomponents, that regulates FSHb expression in response to activation of the cell surface GnRH receptor. LbT2 microarray datasets as well as RNA-Seq data (GSE42120) were interrogated to determine the levels of expression of ALK4/5/7.
2013-11-22 | GSE52631 | GEO
Project description:Lhx8 is a member of the LIM-homeobox transcription factor family and preferentially expressed in oocytes and germ cells within the mouse ovary. We discovered that Lhx8 knockout females lose oocytes within 7 days after birth. At the time of birth, histological examination shows that Lhx8 deficient (Lhx8(-/-)) ovaries are grossly similar to the newborn wild type ovaries. Lhx8(-/-) ovaries fail to maintain the primordial follicles and the transition from primordial to growing follicles does not occur. Lhx8(-/-) ovaries misexpress oocyte-specific genes such as Gdf9, Pou5f1, and Nobox. Very rapid loss of oocytes may partly be due to drastic the down-regulation of Kit and Kitl in Lhx8(-/-) ovaries. We compared Lhx8(-/-) and wild-type ovaries using Affymetrix 430 2.0 microarray platform. Eighty (44%) of 180 of the genes down-regulated more than 5-fold in Lhx8(-/-) ovaries were preferentially expressed in oocytes, whereas only 3 (2%) of 146 genes up-regulated more than 5-fold in the absence of Lhx8 were preferentially expressed in oocytes. In addition, the comparison of genes regulated in Lhx8(-/-) and Nobox(-/-) newborn ovaries discovered a common set of 34 genes whose expression level is affected in both Lhx8 and Nobox deficient mice. Our findings show that Lhx8 is a critical factor for maintenance and differentiation of the oocyte during early oogenesis and it acts in part by down-regulating the Nobox pathway. This SuperSeries is composed of the following subset Series: GSE7774: Transcriptional changes in Lhx8 Null newborn mouse ovaries GSE7775: Microarray Analyses of Newborn Mouse Ovaries Lacking Nobox GSE7776: Ovarian Transcript Expression in Newborn Mouse Refer to individual Series
2008-06-25 | E-GEOD-11897 | biostudies-arrayexpress
Project description:Lhx8 is a member of the LIM-homeobox transcription factor family and preferentially expressed in oocytes and germ cells within the mouse ovary. We discovered that Lhx8 knockout females lose oocytes within 7 days after birth. At the time of birth, histological examination shows that Lhx8 deficient (Lhx8(-/-)) ovaries are grossly similar to the newborn wild type ovaries. Lhx8(-/-) ovaries fail to maintain the primordial follicles and the transition from primordial to growing follicles does not occur. Lhx8(-/-) ovaries misexpress oocyte-specific genes such as Gdf9, Pou5f1, and Nobox. Very rapid loss of oocytes may partly be due to drastic the down-regulation of Kit and Kitl in Lhx8(-/-) ovaries. We compared Lhx8(-/-) and wild-type ovaries using Affymetrix 430 2.0 microarray platform. Eighty (44%) of 180 of the genes down-regulated more than 5-fold in Lhx8(-/-) ovaries were preferentially expressed in oocytes, whereas only 3 (2%) of 146 genes up-regulated more than 5-fold in the absence of Lhx8 were preferentially expressed in oocytes. In addition, the comparison of genes regulated in Lhx8(-/-) and Nobox(-/-) newborn ovaries discovered a common set of 34 genes whose expression level is affected in both Lhx8 and Nobox deficient mice. Our findings show that Lhx8 is a critical factor for maintenance and differentiation of the oocyte during early oogenesis and it acts in part by down-regulating the Nobox pathway. This SuperSeries is composed of the SubSeries listed below.
2008-06-26 | GSE11897 | GEO
Project description:Mouse oocytes control cumulus cell metabolic processes that are deficient in the oocytes themselves and this delegation is necessary for oocyte development. Oocyte-derived bone morphogenetic factor 15 (BMP15) and growth differentiation factor 9 (GDF9) appear to be key regulators of follicular development. The effect of these factors on cumulus cell function before the preovulatory surge of luteinizing hormone (LH) was assessed by analysis of the transcriptomes of cumulus cells from wildtype (WT), Bmp15-/-, and Bmp15-/- Gdf9+/- double mutant (DM) mice using microarray analysis. The biological themes associated with the most highly-affected transcripts were identified using bioinformatic approaches, IPA and GenMAPP/MAPPFinder. There were 5,332, 7,640, and 2,651 transcripts identified to be significantly changed in the comparisons of Bmp15-/- vs. WT, DM vs. WT, and DM vs. Bmp15-/- respectively by the criteria of FC (fold change) p <0.01. Among theses changed transcripts, 744 were commonly changed in all three pair-wise comparisons, and hence were considered to be the most highly affected transcripts by mutation of Bmp15 and Gdf9. IPA Analyses revealed that metabolism was the major theme associated with the most highly-changed transcripts: glycolysis and sterol biosynthesis were the two most significantly affected pathways. Most of the transcripts encoding enzymes for sterol biosynthesis were down-regulated in both mutant cumulus cells and in WT cumulus cell after oocytectomy. Similarly, there was a reduction of de novo-synthesized cholesterol in these cumulus cells. This suggests that oocytes regulate cumulus cell metabolism, particularly sterol biosynthesis, by promoting the expression of corresponding transcripts. Furthermore, in WT-mice, Mvk, Pmvk, Fdps, Sqle, Cyp51, Sc4mol, and Ebp, which encode enzymes in the sterol biosynthetic pathway, were found to be expressed robustly in cumulus cells, but expression was barely detectable in oocytes. Levels of de novo-synthesized cholesterol were significantly higher in cumulusâenclosed oocytes than denuded oocytes. These results indicate that mouse oocytes are deficient in their ability to synthesize cholesterol and require cumulus cells to provide them with products of the sterol biosynthetic pathway. Oocyte-derived BMP15 and GDF9 may promote this metabolic pathway in cumulus cells as compensation for their own deficiencies. Experiment Overall Design: Three sets of independent cumulus cell samples were collected for each genotype (wild type, Bmp15-/-, and Bmp15-/-Gdf9+/-) of mice, and were used for the array study as shown below. Experiment Overall Design: Array Genotype Sample Experiment Overall Design: GC_430_2_GES05_0161_033105_1.CEL WT 1 Experiment Overall Design: GC_430_2_GES05_0162_033105_1.CEL WT 2 Experiment Overall Design: GC_430_2_GES05_0163_033105_1.CEL WT 3 Experiment Overall Design: GC_430_2_GES05_0164_033105_1.CEL Bmp15-/- 4 Experiment Overall Design: GC_430_2_GES05_0165_033105_1.CEL Bmp15-/- 5 Experiment Overall Design: GC_430_2_GES05_0166_033105_1.CEL Bmp15-/- 6 Experiment Overall Design: GC_430_2_GES05_0167_033105_1.CEL DM 7 Experiment Overall Design: GC_430_2_GES05_0168_033105_1.CEL DM 8 Experiment Overall Design: GC_430_2_GES05_0169_033105_1.CEL DM 9
2008-06-15 | E-GEOD-7225 | biostudies-arrayexpress