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Aging-linked deterioration of RNA metabolism destabilizes the stress response of neurons [eCLIP-seq]

ABSTRACT: Aging-linked deterioration of RNA metabolism destabilizes the stress response of neurons [eCLIP-seq]

PROVIDER: PRJNA1159891 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30639400.fastq.gz	Fastqsanger.gz
	SRR30639401.fastq.gz	Fastqsanger.gz
	SRR30639402.fastq.gz	Fastqsanger.gz
	SRR30639403.fastq.gz	Fastqsanger.gz
	SRR30639404.fastq.gz	Fastqsanger.gz

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Aging-linked deterioration of RNA metabolism destabilizes the stress response of neurons [eCLIP-seq]

Project description:Aging is one of the most prominent risk factors for neurodegeneration, yet the molecular mechanisms underlying the deterioration of old neurons are mostly unknown. To efficiently study neurodegeneration in the context of aging, we transdifferentiated primary human fibroblasts from aged healthy donors directly into neurons, which retained their aging markers. Here we show that aged neurons are broadly depleted of RNA-binding proteins, especially spliceosome components. Intriguingly, splicing proteins – like the dementia and ALS-associated protein TDP-43 – mislocalize to the cytoplasm in aged neurons, which leads to widespread alternative splicing. Cytoplasmic spliceosome components typically are recruited to stress granules, but aged neurons suffer from chronic stress that prevents this sequestration. We link chronic stress to the malfunctioning ubiquitylation machinery, poor HSP90α chaperone activity, and the failure to respond to new stress events. Together our data demonstrates that aging-linked deterioration of RNA biology is a key driver of poor resiliency in aged neurons.

2025-02-18 | GSE276985 | GEO

Aging-linked deterioration of RNA metabolism destabilizes the stress response of neurons [RNA-seq]

Project description:Aging-linked deterioration of RNA metabolism destabilizes the stress response of neurons [RNA-seq]

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Aging-linked deterioration of RNA metabolism destabilizes the stress response of neurons [RNASeq, RiboSeq]

Project description:Aging-linked deterioration of RNA metabolism destabilizes the stress response of neurons [RNASeq, RiboSeq]

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Aging-linked deterioration of RNA metabolism destabilizes the stress response of neurons [RNASeq, RiboSeq]

2025-02-18 | GSE277082 | GEO

Aging-linked deterioration of RNA metabolism destabilizes the stress response of neurons [RNA-seq]

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RBM33 eCLIP

Project description:RBM33 eCLIP

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Aging-associated deficit in CCR7 is linked to worsened glymphatic function, cognition and amyloid beta pathology

Project description:Aging leads to a progressive deterioration in brain function, which will eventually result in cognitive decline and can develop into a dementia. The mechanisms underlying pathological cognitive decline in aging are still poorly understood. The peripheral immune system, as well as the meningeal lymphatic vasculature and the immune cells residing in the brain and meninges, are all affected by aging. Moreover, recent studies have linked the dysfunction of the meningeal lymphatic system and peripheral immunity to accelerated brain aging. We hypothesized that an age-related reduction in CCR7-dependent immune cell egress through the lymphatic vasculature mediates some aspects of aging-associated brain dysfunction, leading to cognitive decline and potentially exacerbating neurodegenerative diseases. Here, we report a reduction in CCR7 expression by meningeal T cells in aged mice and its associated increase in meningeal T-regulatory cells. Hematopoietic CCR7 deficiency mimicked the aging-associated changes in meningeal T cells and led to cognitive impairment. Interestingly, CCR7-deficient mice also presented impaired brain glymphatic function and showed increased amyloid beta (A) deposition when crossed with the 5xFAD transgenic mouse model of Alzheimer’s disease (AD). These results show that the aging-associated decrease in CCR7 expression impacts meningeal immunity, affects different aspects of brain function and exacerbates brain A pathology, highlighting its potential as a pathogenic mechanism for cognitive decline in aging and AD.

2021-03-22 | GSE163725 | GEO

Enhanced CLIP uncovers IMP protein-RNA targets in human pluripotent stem cells important for cell adhesion and survival [eCLIP-Seq]

Project description:Human pluripotent stem cells (hPSCs) require precise control of post-transcriptional RNA networks to maintain proliferation and survival. Using a recently developed enhanced UV crosslinking and immunoprecipitation (eCLIP) approach, we identify RNA targets of the IMP/IGF2BP family of RNA-binding proteins in hPSCs. At the broad region- and binding site-level IMP1 and IMP2 show reproducible binding to a large and overlapping set of 3'UTR-enriched targets. RNA Bind-N-Seq applied to recombinant full-length IMP1 and IMP2 reveals CA-rich motifs that are enriched in eCLIP-defined binding sites. We observe that IMP1 loss in hPSCs recapitulates IMP1 phenotypes, including a reduction in cell adhesion and an increase in cell death. For cell adhesion, in hPSCs we find IMP1 maintains levels of integrin mRNA, specifically regulating RNA stability of ITGB5. Additionally, we show IMP1 can be linked to hPSC survival via direct target BCL2. Thus, transcriptome-wide binding profiles identify hPSC targets modulating well-characterized IMP1 roles. eCLIP-seq was performed in biological replicate for IGF2BP1/IMP1 and IGF2BP2/IMP2, as well as one replicate each for IGF2BP3/IMP3, RBFOX2, and an IgG control. Each sample has a size-matched input control for analysis

2016-04-07 | E-GEOD-78507 | biostudies-arrayexpress

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ENO1's RNA-binding sites in Human HeLa cells using eCLIP

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2020-10-27 | E-MTAB-9031 | biostudies-arrayexpress

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