Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA167202 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Chromatin modifier Swi-independent 3a (SIN3A), together with associated histone deacetylases, influences gene expression during development and differentiation through multiple transcription factors in a cell-specific manner. Sin3a is essential for the maintenance of inner cell mass cells of mouse blastocysts, embryonic fibroblasts, and myoblasts, but is not required for the survival of trophectoderm or Sertoli cells. To better understand how this transcriptional regulator modulates cells at different developmental stages within a single lineage, we used conditional gene targeting in mice to ablate Sin3a from perinatal quiescent male gonocytes and from postnatal differentiating spermatogonia. Gene expression in the whole testes of age-matched Ddx4(Vasa/Mvh)-cre mediated conditional Sin3a gene-targeted(VSKO) mice, germ cell-specific Sin3a hemizygous (HEMI) mice, and wild type (WT) mice was measured at postnatal day 0. Two biological replicate animals were used for each condition.
2012-10-01 | E-GEOD-38096 | biostudies-arrayexpress
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:Congenital diaphragmatic hernia (CDH) is a common and severe congential malformation characterized by defects in diaphragm, lung, and pulmonary vascular developent. Despite the frequency and severity of CDH, the underlying developmental mechanisms are not understood. We identified SIN3A loss of function sequence variants in two patients with CDH. To understand the genetic and developmental mechanisms of CDH, we generated Sin3a conditional knockout mice that lack Sin3a expression in the lung mesenchyme. SIN3A plays a critcal role during development, directing cell lineage specification and cell cycling. Despite this role, SIN3A sequence variants have not been reported in patients with CDH or other congential malformations. We found that Sin3a CKO mice have abnormal lung stucture at birth into adulthood. To determine the role of Sin3a in lung mesenchymal development, we performed transcriptomic analysis of Sin3a CKO and control lungs at embryonic day 16 (E16) when cell cycling defects were first evident, postnatal day 0 (P0) when lung defects were first evident, and P3 when lung phenotyopes worsened. In this dataset are expression data from dissected embryonic and postnatal lungs of Sin3a CKO and control mice. Sin3a CKO mice have conditional deletion of Sin3a in the lung mesenchyme directed by Tbx4rtta; tetocre (Tbx4rtta; tetocre; Sin3a flox/flox CKO). Control mice are heterozygous for Sin3a in the lung mesenchyme (Tbx4rtta; tetocre; Sin3a flox/WT). These data were used to identify transcriptional changes due to loss of Sin3a in the lung mesenchyme.
2023-12-31 | GSE246305 | GEO
Project description:MicroRNAs (miRNAs) are a class of endogenous, non-coding RNAs that mediate post-transcriptional gene silencing by inhibiting mRNA translation and promoting mRNA decay. DICER1, an RNAse III endonuclease encoded by Dicer1, is required for processing short 21-22 nucleotide miRNAs from longer double-stranded RNA precursors. Here, we investigate the loss of Dicer1 in mouse postnatal male germ cells to determine how disruptions in the miRNA biogenesis pathway may contribute to infertility. Reduced levels of Dicer1 transcripts and DICER1 were confirmed in germ cell knock-out (GCKO) testes by postnatal day 18 (P18). Compared to wild-type (WT) at 8 weeks, GCKO males had no change in body weight, yet showed significant reductions in testis mass and sperm number. Histology and fertility tests confirmed spermatogenic failure in GCKO males. Array analyses at P18 showed 96% of miRNA genes were down-regulated and 37% of protein-coding genes were differentially expressed in GCKO testes. Interestingly, we observed preferential overexpression of genes on the sex chromosomes in GCKO testes, with more than 80% of the genes overlapping those proposed to undergo meiotic sex chromosome inactivation (MSCI) in the germ cells. Compared to WT, GCKO mice showed higher percentages of cells at early meiotic stages (leptotene and zygotene) but lower percentages at later stages (pachytene, diplotene and metaphase I), providing evidence that deletion of Dicer1 leads to disruptions in meiotic progression. Furthermore, we observed fewer elongating spermatids with proper translational activation of transition protein 2 (Tnp2), protamine 1 and 2 (Prm1 and Prm2) in GCKO testes after step 12-14. Therefore, deleting Dicer1 in early postnatal germ cells causes misregulation of transcripts encoded by genes on the sex chromosomes, impairs meiotic progression and post-meiotic translational control and results in spermatogenic failure and infertility. Total RNA, including miRNAs, were purified from a total of six individual mouse samples. The tissue collected was obtained from wild-type (control; n=3) and Dicer1 germ cell knockout (mutant; n=3) testes on P18.
2012-09-10 | E-GEOD-38891 | biostudies-arrayexpress
Project description:This is a study to explore the transcriptional changes after cadmium treatment in adult rat testes at three time points (control--0 hour, 8 hour and 4 day). Cadmium is an environmental toxicant that is known to affect the male reproductive system. It disrupts the blood-testis barrier irreversibly, and affects the Sertoli-germ cells adhesion, causing germ cell depletion from the seminiferous epithelium. Keywords: Cadmium effect in rat testes
2007-11-07 | GSE9480 | GEO
Project description:To investigate the role of DDX20 in spermatogenesis, we generated Ddx20 flox/flox Ddx4-Cre mice to make a germ cell-specific Ddx20 knockout, and isolated spermatogonia from four-day-old mouse testes by THY1 magnetic beads. We then performed proteomic analysis using protein lysates obtained from THY1 + spermatogonia.
2024-04-24 | PXD038170 | iProX
Project description:MicroRNAs (miRNAs) are a class of endogenous, non-coding RNAs that mediate post-transcriptional gene silencing by inhibiting mRNA translation and promoting mRNA decay. DICER1, an RNAse III endonuclease encoded by Dicer1, is required for processing short 21-22 nucleotide miRNAs from longer double-stranded RNA precursors. Here, we investigate the loss of Dicer1 in mouse postnatal male germ cells to determine how disruptions in the miRNA biogenesis pathway may contribute to infertility. Reduced levels of Dicer1 transcripts and DICER1 were confirmed in germ cell knock-out (GCKO) testes by postnatal day 18 (P18). Compared to wild-type (WT) at 8 weeks, GCKO males had no change in body weight, yet showed significant reductions in testis mass and sperm number. Histology and fertility tests confirmed spermatogenic failure in GCKO males. Array analyses at P18 showed 96% of miRNA genes were down-regulated and 37% of protein-coding genes were differentially expressed in GCKO testes. Interestingly, we observed preferential overexpression of genes on the sex chromosomes in GCKO testes, with more than 80% of the genes overlapping those proposed to undergo meiotic sex chromosome inactivation (MSCI) in the germ cells. Compared to WT, GCKO mice showed higher percentages of cells at early meiotic stages (leptotene and zygotene) but lower percentages at later stages (pachytene, diplotene and metaphase I), providing evidence that deletion of Dicer1 leads to disruptions in meiotic progression. Furthermore, we observed fewer elongating spermatids with proper translational activation of transition protein 2 (Tnp2), protamine 1 and 2 (Prm1 and Prm2) in GCKO testes after step 12-14. Therefore, deleting Dicer1 in early postnatal germ cells causes misregulation of transcripts encoded by genes on the sex chromosomes, impairs meiotic progression and post-meiotic translational control and results in spermatogenic failure and infertility. Total RNA, including miRNAs, were purified from a total of six individual mouse samples. The tissue collected was obtained from wild-type (control; n=3) and Dicer1 germ cell knockout (mutant; n=3) testes on P18. One miRNA GCKO sample, M36, was determined to be of poor quality and was excluded from the study; thus, a total of five miRNA samples were analyzed.
2012-09-10 | E-GEOD-38895 | biostudies-arrayexpress
Project description:The ability of male reproduction is seriously dependent on Sertoli cells. However, the mechanisms governing the functional integrity of Sertoli cells remained largely unexplored. Tyrosine phosphatase protein Shp2 is expressed in germ, Leydig and Sertoli cells of mice testes. But the physiological role of Shp2 in the spermatogenesis was not fully understood. Thus, we conditionally deleted Shp2 gene in Sertoli cells using two transgenic models, and demonstrated that Shp2 deficiency caused infertility, excessive differentiation of SSCs and abnormal BTB in mice. To further discover the underlying mechanism of Shp2 regulation, we collected the mRNA of testes from wild type or knockout mice at 16.5 fetal day, Postnatal 3 days, 1 weeks, 2 weeks, and then screened the gene expression.
2015-05-14 | GSE68829 | GEO
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.
2010-04-27 | GSE21525 | GEO
Project description:The ability of male reproduction is seriously dependent on Sertoli cells. However, the mechanisms governing the functional integrity of Sertoli cells remained largely unexplored. Tyrosine phosphatase protein Shp2 is expressed in germ, Leydig and Sertoli cells of mice testes. But the physiological role of Shp2 in the spermatogenesis was not fully understood. Thus, we conditionally deleted Shp2 gene in Sertoli cells using two transgenic models, and demonstrated that Shp2 deficiency caused infertility, excessive differentiation of SSCs and abnormal BTB in mice. To further discover the underlying mechanism of Shp2 regulation, we collected the mRNA of testes from wild type or knockout mice at 16.5 fetal day, Postnatal 3 days, 1 weeks, 2 weeks, and then screened the gene expression. Testis tissues from Shp2f/f and SCSKO mice were for RNA extraction and hybridization on Affymetrix microarrays.
2015-05-14 | E-GEOD-68829 | biostudies-arrayexpress