Abnormal H3K27me3 underlies degenerative spermatogonial stem cells in cryptorchid testis [ChIP-Seq]
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1186234 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR31357042_1.fastq.gz | Fastqsanger.gz | |||
| SRR31357042_2.fastq.gz | Fastqsanger.gz | |||
| SRR31357043_1.fastq.gz | Fastqsanger.gz | |||
| SRR31357043_2.fastq.gz | Fastqsanger.gz | |||
| SRR31357044_1.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:Abnormal H3K27me3 underlies degenerative spermatogonial stem cells in cryptorchid testis [RNA-Seq]
| PRJNA1186236 | ENA
Project description:Cryptorchidism is the most frequent congenital defect in newborn males characterized by the absence of the testis from the scrotum. Approximately 90% of patients with untreated bilateral cryptorchidism exhibit azoospermia due to defective spermatogenesis in the affected testis. While abnormal spermatogonial stem cell maintenance or differentiation is suggested to cause germ cell degeneration in the cryptorchid testis, underlying molecular mechanisms remain unclear. Here we profiled spermatogonial epigenetic landscapes using surgically induced cryptorchid testis in the mouse. We show that cryptorchidism leads to alterations in local, but not global H3K27me3 and H3K9me3 in undifferentiated spermatogonia. Of these, the loss of H3K27me3 leads to activation of developmental and apoptotic pathway genes that are repressed by the polycomb machineries in germ cells. Cryptorchid spermatogonia exhibit the increase of H3K27me3 demethylases KDM6A and KMD6B. Furthermore, we reveal that an increased temperature leads to Kdm6a/b upregulation in germline stem cells cultured in vitro. Thus, our study suggests that a temperature-dependent histone demethylation induces mRNA dysregulation due to the partial loss of H3K27me3 in spermatogonia.
2024-12-25 | GSE281948 | GEO
Project description:Cryptorchidism is the most frequent congenital defect in newborn males characterized by the absence of the testis from the scrotum. Approximately 90% of patients with untreated bilateral cryptorchidism exhibit azoospermia due to defective spermatogenesis in the affected testis. While abnormal spermatogonial stem cell maintenance or differentiation is suggested to cause germ cell degeneration in the cryptorchid testis, underlying molecular mechanisms remain unclear. Here we profiled spermatogonial epigenetic landscapes using surgically induced cryptorchid testis in the mouse. We show that cryptorchidism leads to alterations in local, but not global H3K27me3 and H3K9me3 in undifferentiated spermatogonia. Of these, the loss of H3K27me3 leads to activation of developmental and apoptotic pathway genes that are repressed by the polycomb machineries in germ cells. Cryptorchid spermatogonia exhibit the increase of H3K27me3 demethylases KDM6A and KMD6B. Furthermore, we reveal that an increased temperature leads to Kdm6a/b upregulation in germline stem cells cultured in vitro. Thus, our study suggests that a temperature-dependent histone demethylation induces mRNA dysregulation due to the partial loss of H3K27me3 in spermatogonia.
2024-12-25 | GSE281946 | GEO
Project description: Not available
| S-EPMC11829757 | biostudies-literature
Project description:Disc Degeneration is a multifactorial disease which cause severe constant chronic pain. The development of disc degeneration could involve both genetic and environmental factors, so it's important to elucidate the difference in gene expression profiles between degenerative and non-degenerative discs from elderly patients and younger patients, respectively. Affymetrix GeneChip Human Genome U133A Array was used to derive gene expression profiles and identified genes that would express at significantly different levels between degenerative and non-degenerative samples. Human intervertebral disc tissues were harvested from elderly and younger patients with degenerative disc disease and adolescent idiopathic scoliosis, respectively, for RNA extraction and hybridization on Affymetrix microarrays. One degenerative sample was compared to one non-degenerative sample in the same microarray run, and comparative analyses were performed in triplicate. Gene whose expression levels varied across the samples with a log ratio >0.5 or <-0.5 were selected as the genes related to disc degeneration.
2012-05-31 | E-GEOD-34095 | biostudies-arrayexpress
Project description:A disrupted compartment boundary underlies abnormal cardiac patterning and congenital heart defects
| PRJNA1082312 | ENA
Project description:Disc Degeneration is a multifactorial disease which cause severe constant chronic pain. The development of disc degeneration could involve both genetic and environmental factors, so it's important to elucidate the difference in gene expression profiles between degenerative and non-degenerative discs from elderly patients and younger patients, respectively. Affymetrix GeneChip Human Genome U133A Array was used to derive gene expression profiles and identified genes that would express at significantly different levels between degenerative and non-degenerative samples.
2012-06-01 | GSE34095 | GEO
Project description:Protein dephosphorylation mediated by phosphatases regulates spermatogenesis. However, which proteins are dephosphorylated and how they regulate spermatogenesis are largely unknown. Here, we show that germline-specific deletion of protein phosphatase 6 regulatory subunit 3 (PPP6R3), which determines substrate specificity of protein phosphatase 6 catalytic subunit, causes abnormal spermatogonial differentiation and male infertility, accompanied by translation inhibition. PPP6R3 directly interacts with EIF3C and EIF4G1 in KIT+ spermatogonia. Decreased levels of non-phosphorylated EIF3C and EIF4G1 after PPP6R3 deletion attenuate their enrichment for mRNAs associated with spermatogonial differentiation, and increased phosphorylation levels promote their degradation. Specifically, the phosphorylation status both of EIF3CS39 and EIF4G1S1217 are significantly upregulated in mutant mice. Overexpression of EIF3CS39A and EIF4G1S1217A mutants in Ppp6r3-cKO spermatogonial progenitor cells compensates for their differentiation efficiency by upregulating the translation rates of differentiation-associated mRNAs. Our findings demonstrate that dephosphorylation of EIF3C and EIF4G1 mediated by PPP6R3 is critical for translation activation during spermatogonial differentiation.
2025-06-20 | GSE278121 | GEO
Project description:In vitro and in vivo aging of mouse spermatogonial stem cells alters stem cell function based on quantitative spermatogonial stem cell transplantation analyses. We used microarrays to identify differential gene expression in vitro and in vivo aged spermatogonial stem cells to identify potential causes of observed phenotypic differences in aged spermatogonial stem cell function. Spermatogonial stem cells were isolated from young and serial-transplanted aged mouse donors and cultured for short and long periods. Spermatogonial stem cells were isolated from cultures and subjected to microarray analysis to identify differential gene expression.
2011-02-04 | E-GEOD-27043 | biostudies-arrayexpress
Project description:Background: Spermatogonial stem cells (SSCs) sustain the process of steady-state spermatogenesis in the mammalian testis, which is critical to the ongoing production of sperm and male fertility. SSCs can both self-renew to perpetuate the SSC population, and give rise to progenitors to propel the spermatogenic differentiation pathway. SSCs are detectable as a small subpopulation of undifferentiated spermatogonia that demonstrate regenerative capacity in a transplantation assay, and can be selectively recovered on the basis of expression of an Id4-eGfp sortable marker transgene. Enriched populations of SSCs and progenitors display consistent differences in gene expression patterns suggesting they represent discrete spermatogonial subtypes. Results: Here we describe distinct spermatogonial subtype-specific epigenetic programming profiles associated with subtype-specific differential gene expression on the basis of genome-wide patterns of six different histone modifications, chromatin accessibility, and DNA methylation. We find that similarly expressed genes show no differences in epigenetic programming, whereas differentially expressed genes show distinct histone modification patterns as well as subtype-specific differences in patterns of distal intergenic low-methylated regions. Motif-enrichment analysis of differentially programmed elements predicts a set of transcription factors that may regulate this spermatogonial subtype-specific epigenetic programming, and gene-specific chromatin immunoprecipitation analyses confirm subtype-specific differences in binding of a subset of these factors to target genes. Conclusions: Taken together, these results indicate that SSCs and progenitors are discrete spermatogonial subtypes that appear to be differentially programmed to carry out mutually exclusive functions including self-renewal and maintenance of regenerative capacity in SSCs and lineage commitment and loss of regenerative capacity in progenitors.
2019-05-23 | GSE131656 | GEO