Expression data from testis of day-7 Sohlh1 knock-out mice
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE21525 | GEO | 2010/04/27
SECONDARY ACCESSION(S): PRJNA125951
REPOSITORIES: GEO
Similar Datasets
Project description:Sohlh1 and Sohlh2 encode a germ cell-specific basic helix-loop-helix transcriptional regulator critical in spermatogonial differentiation. Seven-day-old Sohlh1 or Sohlh2 knockout and wild-type testes were arrayed on the Affy 430 2.0 platform. The following mice were analyzed at postnatal day 7: wild-type, Sohlh1-/-, and Sphlh2-/-. 4 samples/group.
2010-05-07 | E-GEOD-21525 | 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: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. 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: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.
2010-10-22 | GSE24816 | GEO
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: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
Project description:In mammals, a key transition in spermatogenesis is the exit from spermatogonial differentiation and mitotic proliferation and the entry into spermatocyte differentiation and meiosis. Although several genes that regulate this transition have been identified, how it is controlled and coordinated remains poorly understood. Here we examine the role in male gametogenesis of the Doublesex-related gene Dmrt6 (Dmrtb1) and find that Dmrt6 plays a critical role in directing germ cells through the mitotic to meiotic germ cell transition. DMRT6 protein is expressed in late mitotic spermatogonia. In mice of the C57BL/6J strain a null mutation in Dmrt6 disrupts spermatogonial differentiation, causing expression in inappropriate cell types of spermatogonial differentiation factors including SOHLH1, SOHLH2 and DMRT1 and the meiotic initiation factor STRA8 and causing most late spermatogonia to undergo apoptosis. In mice of the 129Sv background, most Dmrt6 mutant spermatogonia can complete differentiation and enter meiosis, but they show defects in chromosome pairing, establishment of the XY body, and processing of recombination foci, and mainly arrest in mid-pachynema. mRNA profiling of Dmrt6 mutant testes together with DMRT6 ChIP-seq suggest that DMRT6 represses genes involved in spermatogonial differentiation and activates genes required for meiotic prophase. Our results indicate that Dmrt6 plays a key role in coordinating the transition in gametogenic programs from spermatogonial differentiation and mitosis to spermatocyte development and meiosis. Six samples for RNA-Seq with three biological replicates in each group. Two samples for ChIP-Seq (one input and one ChIP).
2014-10-31 | E-GEOD-60440 | biostudies-arrayexpress
Project description:In mammals, a key transition in spermatogenesis is the exit from spermatogonial differentiation and mitotic proliferation and the entry into spermatocyte differentiation and meiosis. Although several genes that regulate this transition have been identified, how it is controlled and coordinated remains poorly understood. Here we examine the role in male gametogenesis of the Doublesex-related gene Dmrt6 (Dmrtb1) and find that Dmrt6 plays a critical role in directing germ cells through the mitotic to meiotic germ cell transition. DMRT6 protein is expressed in late mitotic spermatogonia. In mice of the C57BL/6J strain a null mutation in Dmrt6 disrupts spermatogonial differentiation, causing expression in inappropriate cell types of spermatogonial differentiation factors including SOHLH1, SOHLH2 and DMRT1 and the meiotic initiation factor STRA8 and causing most late spermatogonia to undergo apoptosis. In mice of the 129Sv background, most Dmrt6 mutant spermatogonia can complete differentiation and enter meiosis, but they show defects in chromosome pairing, establishment of the XY body, and processing of recombination foci, and mainly arrest in mid-pachynema. mRNA profiling of Dmrt6 mutant testes together with DMRT6 ChIP-seq suggest that DMRT6 represses genes involved in spermatogonial differentiation and activates genes required for meiotic prophase. Our results indicate that Dmrt6 plays a key role in coordinating the transition in gametogenic programs from spermatogonial differentiation and mitosis to spermatocyte development and meiosis.
2014-10-31 | GSE60440 | GEO
