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Changes in global gene expression patterns caused by acute deletion of TERT in spermatogonial stem cells

ABSTRACT: Changes in global gene expression patterns caused by acute deletion of TERT in spermatogonial stem cells

PROVIDER: PRJNA607811 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11127434_1.fastq.gz	Fastqsanger.gz
	SRR11127434_2.fastq.gz	Fastqsanger.gz
	SRR11127435_1.fastq.gz	Fastqsanger.gz
	SRR11127435_2.fastq.gz	Fastqsanger.gz
	SRR11127436_1.fastq.gz	Fastqsanger.gz

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Changes in global gene expression patterns caused by acute deletion of TERT in spermatogonial stem cells

Project description:To understand the catalytic activity-independent functions of TERT in global gene expression, we acutely deleted TERT in spermatogonial stem cells in the testis, and performed RNA-seq. We find significant down-regulation of MYC pathway genes in TERT-deleted SSCs.

2024-07-11 | GSE145655 | GEO

Changes in global open chromatin structure caused by acute deletion of TERT in spermatogonial stem cells

Project description:To understand the catalytic activity-independent functions of TERT in global chromatin structure, we acutely deleted TERT in spermatogonial stem cell (SSC) populations in the testis, and performed ATAC-seq. We find significant global loss of open chromatin structure in TERT-deleted SSC populations.

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Changes in global open chromatin structure caused by acute deletion of TERT in spermatogonial stem cells

Project description:Changes in global open chromatin structure caused by acute deletion of TERT in spermatogonial stem cells

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PITX1 suppresses TERT transcription

Project description:Using microcell-mediated chromosome transfer (MMCT) into the mouse melanoma cell line, B16F10, we have previously found that human chromosome 5 carries a gene, or genes, that can negatively regulate TERT expression. To identify the gene responsible for the regulation of TERT transcription, we performed cDNA microarray analysis using parental B16F10 cells, telomerase negative B16F10 microcell hybrids with a human chromosome 5 (B16F10MH5), and its revertant clones (MH5R) with reactivated telomerase. Here we report the identification of PITX1, whose restoration leads to the downregulation of mouse tert (mtert) transcription, as a TERT suppressor gene. Additionally, both human TERT (hTERT) and mouse TERT (mtert) promoter activity can be suppressed by PITX1. We showed that three and one binding sites, respectively, within the hTERT and mtert promoters that express a unique conserved region are responsible for the transcriptional activation of TERT. Furthermore, we showed that PITX1 binds to the TERT promoter both in vitro and in vivo. Thus, PITX1 suppresses TERT transcription through direct binding to the TERT promoter, which ultimately regulates telomerase activity.

2010-09-10 | GSE23216 | GEO

Expression data from aged spermatogonial stem cells

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.

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DIS3L2 is an essential regulator of spermatogonial differentiation in mice

Project description:Using conditional knockout mice model, here we report the essential role of DIS3L2 in regulating male germline proliferation, growth and differentiation to ensure male fertility. We document that DIS3L2 is essential for spermatogonial homeostasis. DIS3L2-specific deletion in spermatogonia results in the reduction of the undifferentiated spermatogonial population and the block in transition to the differentiating stage in postnatal testes.

2021-07-15 | GSE160104 | GEO

PITX1 suppresses TERT transcription

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Genome-wide analysis of TERT-AD mouse cortical and hippocampal neurons upon Tert activation

Project description:Analysis of TERT-regulated global gene expression changes. The hypothesis tested in the present study was that neuronal TERT influences the regulation of gene expressions. Results provide important information of the response of in vivo mouse neurons to physiological TERT induction.

2021-10-12 | GSE163523 | GEO

ROS amplification drives mouse spermatogonial stem cell self-renewal

Project description:Reactive oxygen species (ROS) play critical roles in self-renewal division for various stem cell types. However, it remains unclear how ROS signals are integrated with selfrenewal machinery. Here we report that the MAPK14/MAPK7/BCL6B pathway creates a positive feedback loop to drive spermatogonial stem cell (SSC) self-renewal via ROS amplification. The activation of MAPK14 induced MAPK7 phosphorylation in cultured SSCs, and targeted deletion of Mapk14 or Mapk7 resulted in significant SSC deficiency after spermatogonial transplantation. The activation of this signaling pathway not only induced Nox1 but also increased ROS levels. Chemical screening of MAPK7 targets revealed many ROS-dependent spermatogonial transcription factors, of which BCL6B was found to initiate ROS production by increasing Nox1 expression via ETV5-induced nuclear translocation. Because hydrogen peroxide or Nox1 transfection also induced BCL6B nuclear translocation, our results suggest that BCL6B initiates and amplifies ROS signals to activate ROS-dependent spermatogonial transcription factors by forming a positive feedback loop.

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Project description:Point mutations within the TERT promoter are the most common recurrent somatic non-coding mutation identified across different cancer types, including glioblastoma, melanoma, hepatocellular carcinoma and bladder cancer. They are most abundant at C146T and C124T and more rare at A57C, with the latter originally described as a familial case but subsequently shown also to occur somatically. All three mutations create de novo ETS (E-twenty-six specific) binding sites and result in the reactivation of the TERT gene, allowing cancer cells to achieve replicative immortality. Here, we employed a systematic proteomics screen to identify transcription factors preferentially binding to the C146T, C124T and A57C mutations. While we confirmed binding of multiple ETS factors to the mutant C146T and C124T sequences, we identified E4F1 a an A57C-specific binder and ZNF148 as a TERT WT binder that is excluded from the TERT promoter by the C124T allele. Both proteins are activating transcription factors that bind specifically to the A57C and wildtype (at position 124) TERT promoter sequence in corresponding cell lines and upregulate TERT transcription and telomerase activity.

2023-11-04 | PXD037776 | Pride

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