Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA133643 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:This SuperSeries is composed of the following subset Series: GSE24815: Transcriptional changes in Sohlh1/Sohlh2 double knockout mouse newborn ovaries GSE24816: Transcriptional changes in Sohlh1 knockout and Sohlh2 knockout mouse newborn ovaries Refer to individual Series
2010-10-22 | E-GEOD-24817 | biostudies-arrayexpress
Project description:Transcriptional changes in Sohlh1 knockout and Sohlh2 knockout mouse newborn ovaries
| PRJNA133645 | ENA
Project description:Sohlh1 and Sohlh2 are germ cell-specific basic helix-loop-helix transcription factors critical in early folliculogenesis. Differential genes expression by both Sohlh1 and Sohlh2 deficiency in mouse newborn ovaries was accessed using microarray. RNA samples from Sohlh1/ Sohlh2 double knockout and wild-type newborn ovaries were arrayed on the Illumina beadchip mouse WG-6 2.0. Total RNA isolated from wildtype and Sohlh1/Sohlh2 double KO mouse newborn ovary were used to run Illumina BeadChip MouseWG-6 2.0 arrays.
2010-10-22 | E-GEOD-24815 | biostudies-arrayexpress
Project description:Sohlh1 and Sohlh2 are germ cell-specific basic helix-loop-helix transcription factors critical in early folliculogenesis. Differential genes expression by both Sohlh1 and Sohlh2 deficiency in mouse newborn ovaries was accessed using microarray. RNA samples from Sohlh1/ Sohlh2 double knockout and wild-type newborn ovaries were arrayed on the Illumina beadchip mouse WG-6 2.0.
2010-10-22 | GSE24815 | GEO
Project description:Transcriptional changes in Lhx8 Null newborn mouse ovaries
| PRJNA109017 | ENA
Project description:Sohlh1 and Sohlh2 are germ cell-specific basic helix-loop-helix transcription factors critical in early folliculogenesis. We discovered that Sohlh1 and Sohlh2 knockout females lose oocytes after birth and few remains by postnatal day 14. Here, we show that many genes preferentially expressed in the oocytes are misregulated by Sohlh1 and/or Sohlh2 deficiency. Total RNA samples isolated from wildtype, Sohlh1 KO and Sohlh2 KO mouse newborn ovaries were arrayed on the Illumina BeadChip MouseWG-6 2.0 arrays. We have 4 replicates for wildtype and Sohlh1 KO and 3 replicates for Sohlh2 KO.
2010-10-22 | E-GEOD-24816 | biostudies-arrayexpress
Project description:Microarray Analyses of Newborn Mouse Ovaries Lacking Nobox
| PRJNA109019 | ENA
Project description:We discovered that expression of the transcription factor RUNX1 is enriched in the fetal ovary in various vertebrate species. In the mouse, RUNX1 marks the supporting cell lineage and becomes granulosa cell-specific as the gonads differentiate. To understand the function of Runx1 during fetal development of the ovary, we ablated Runx1 specifically in the somatic cell lineage of the fetal ovaries using Sf1-Cre . We compared ovarian differentiation in wild type, Runx1 and Foxl2 single knockouts, and Runx1/Foxl2 double knockout ovaries. Transcriptome comparisons of newborn ovaries revealed that loss of Runx1 or Foxl2 affected a similar set of genes: 41% of the genes affected by the loss of Runx1 were also changed by the loss of Foxl2. Despite these transcriptomic changes, granulosa cell identity was maintained during fetal life in both Runx1 or Foxl2 single knockout ovaries. However, the combined loss of Runx1/Foxl2 resulted in masculinization of the ovaries during fetal life. To further characterize the impacts of the combined loss of Runx1 and Foxl2 on ovarian differentiation, we compared the transcriptome of Runx1/Foxl2 DKO newborn ovaries with the transcriptomes of control, Runx1, or Foxl2 single KO ovaries.
2019-07-17 | GSE129038 | 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:Germ-cell transcription factors control gene networks that regulate primordial follicle formation and oocyte differentiation during early, postnatal mouse oogenesis. Taking advantage of gene-edited mice lacking transcription factors expressed in female germ cells, we analyzed global gene expression profiles in perinatal ovaries from wildtype, FiglaNull, Lhx8Null and SohlhNull mice. Figla deficiency dysregulates expression of meiosis-related genes (e.g., Sycp3, Rad51 and Msy2) and a variety of genes (e.g., Nobox, Lhx8, Taf4b, Sohlh1, Sohlh2 and Gdf9) associated with oocyte growth and differentiation. The absence of FIGLA significantly impedes meiotic progression, causes DNA damage and results in oocyte apoptosis. Moreover, we find that FIGLA and other transcriptional regulators (e.g., NOBOX, LHX8, SOHLH1 and SOHLH2) are co-expressed in the same subset of germ cells in perinatal ovaries and Figla ablation dramatically disrupts KIT, NOBOX, LHX8, SOHLH1 and SOHLH2 expression. In addition, not only do FIGLA, SOHLH1 and LHX8 cross-regulate each other, they also cooperate by direct interaction with each during early oocyte development and share downstream gene targets. Thus, our findings substantiate a major role for FIGLA, LHX8 and SOHLH1 as multifunctional regulators of networks necessary for oocyte maintenance and differentiation during early folliculogenesis.
2019-11-06 | GSE139966 | GEO