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Aging of mouse spermatogonial stem cells by Wnt7b-Jnk pathway activation [ChIP-seq]

ABSTRACT: Aging of mouse spermatogonial stem cells by Wnt7b-Jnk pathway activation [ChIP-seq]

PROVIDER: PRJNA494505 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7958270.fastq.gz	Fastqsanger.gz
	SRR7958271.fastq.gz	Fastqsanger.gz
	SRR7958272.fastq.gz	Fastqsanger.gz
	SRR7958273.fastq.gz	Fastqsanger.gz
	SRR7958274.fastq.gz	Fastqsanger.gz

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Aging of mouse spermatogonial stem cells by Wnt7b-Jnk pathway activation [ChIP-seq]

Project description:Because spermatogonial stem cells (SSCs) are virtually immortal by serial transplantation, SSC decrease in aged testes is considered to be caused by deteriorated microenvironment. Here we report cell-intrinsic mode of SSC aging. SSCs cultured for 5 years proliferate more actively than young SSCs and showed enhanced glycolytic activity but remain euploid and exhibited stable androgenetic imprinting patterns. Moreover, the aged SSCs kept constant SSC activity despite shortened telomeres. The increased proliferative activity of aged SSCs was caused by Wnt7b expression, which likely occurred due to decreased polycomb complex2 activity. Aberrant Wnt7b expression not only decreased reactive oxygen species levels and mitochondria activity but also stimulated glycolysis via c-jun N-terminal kinase (JNK) activation. Analysis of SSCs in Klotho aging mouse model also confirmed hyperactivation of JNK pathway and increased glycolysis. Therefore, not only SSC microenvironment but also intrinsic activation of Wnt7b-mediated glycolysis plays important roles in SSC aging.

2019-07-30 | GSE120777 | GEO

Aging of mouse spermatogonial stem cells by Wnt7b-Jnk pathway activation [Bisulfite-seq]

2019-07-30 | GSE120775 | GEO

Aging of mouse spermatogonial stem cells by Wnt7b-Jnk pathway activation

Project description:Aging of mouse spermatogonial stem cells by Wnt7b-Jnk pathway activation

| PRJNA494503 | ENA

Aging of mouse spermatogonial stem cells by Wnt7b-Jnk pathway activation [Bisulfite-seq]

Project description:Aging of mouse spermatogonial stem cells by Wnt7b-Jnk pathway activation [Bisulfite-seq]

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Project description:Aging of mouse spermatogonial stem cells by Wnt7b-Jnk pathway activation

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Expression data from aging study on mouse spermatogonial stem/progenitor cell population

Project description:In mouse, spermatogonial stem/progenitor cells are the progenitor cell which develop to mature sperms through a series of mitotic and meiotic divisions and differentiation. Gfra1 is an established surface marker for mouse spermatogonial stem/progenitor cells. In this study, we used a transcriptomic approach to investigate the effect of aging on Gfra1-positive and -negative populations of mouse male germ cells. Spermatogonial stem/progenitor cells were isolated from testes of mice at ages 6-day, 21-day, 60-day, and 8-months by magnetic assisted cell sorting (MACS) technique using Gfra1 marker. Transcriptomes among different ages and Gfra1 status were compared.

2015-05-24 | E-GEOD-68298 | biostudies-arrayexpress

Aging of mouse spermatogonial stem cells by Wnt7b-Jnk pathway activation

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-07-30 | GSE120778 | GEO

Aging of spermatogonial stem cells by Jnk-mediated glycolysis activation.

Project description:Because spermatogonial stem cells (SSCs) are immortal by serial transplantation, SSC aging in intact testes is considered to be caused by a deteriorated microenvironment. Here, we report a cell-intrinsic mode of SSC aging by glycolysis activation. Using cultured SSCs, we found that aged SSCs proliferated more actively than young SSCs and showed enhanced glycolytic activity. Moreover, they remained euploid and exhibited stable androgenetic imprinting patterns with robust SSC activity despite having shortened telomeres. Aged SSCs showed increased Wnt7b expression, which was associated with decreased Polycomb complex 2 activity. Our results suggest that aberrant Wnt7b expression activated c-jun N-terminal kinase (JNK), which down-regulated mitochondria numbers by suppressing Ppargc1a Down-regulation of Ppargc1a probably decreased reactive oxygen species and enhanced glycolysis. Analyses of the Klotho-deficient aging mouse model and 2-y-old aged rats confirmed JNK hyperactivation and increased glycolysis. Therefore, not only microenvironment but also intrinsic activation of JNK-mediated glycolysis contributes to SSC aging.

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CRKL enhances YAP signaling through binding and JNK/JUN pathway activation in liver cancer

Project description:Hepatocellular carcinoma (HCC) presents a major health issue due to its rising incidence and limited therapeutic options. The Hippo pathway transducers yes-associated protein (YAP) and WW-domain containing transcription regulator 1 (WWTR1/TAZ) are key regulators of liver tu-morigenesis promoting tumor formation and progression. Although first inhibitors are in clinical trials, targeting the upstream activation of YAP/TAZ could prove equally beneficial. To identify regulators of YAP/TAZ activity, we carried out a proximity labelling approach (BioID) coupled to mass-spectrometry. We verified CRKL as a new YAP-exclusive interaction partner, which is overexpressed in HCC patients correlating with YAP expression and activity as well as poor survival prognosis. In vitro experiments demonstrated CRKL dependent cell survival and loss of YAP binding induced through actin disruption. Moreover, we delineated an activation of the JNK/JUN pathway by CRKL, which promoted YAP transcription. Our data thus illustrated that CRKL not only promoted YAP activity through its binding but also through the induction of YAP transcription by JNK/JUN activation. This highlights the JNK/JUN pathway as a possible target to abrogate YAP expression in HCC patients.

2024-11-26 | PXD058235 | Pride

Transient inhibition of JNK pathway improves hematopoietic stem cell engraftment

Project description:We found that transient inhibition of JNK pathway increased short term-HSC frequency in cord blood CD34+ cells by 12.56 folds. Transcriptome analysis shows that inhibition of JNK pathway upregulated HSC-specific and anti-oxidative gene expression, prevented upregulation of cell cycle entry, oxidative phosphorylation and glycolysis related gene expression, and downregulated reactive oxygen species (ROS) active gene expression. Consistently, cell cycle and metabolic analysis show that inhibition of JNK pathway prevented HSC from cell cycle entry, glucose uptake increase and ROS accumulation. Accordingly, transient inhibition of JNK pathway also enhanced long term-HSC recovery during cord blood CD34+ cell collection. Collectively, these findings suggest that transient inhibition of JNK pathway could promote quiescent state of HSCs by preventing cell cycle entry and metabolic activation, thus improving HSC recovery and engraftment ability.

2022-06-29 | GSE165501 | GEO

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