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Telomere-to-mitochondria signaling by ZBP1 mediates replicative crisis

ABSTRACT: Telomere-to-mitochondria signaling by ZBP1 mediates replicative crisis

PROVIDER: PRJNA903482 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22351301.fastq.gz	Fastqsanger.gz
	SRR22351302.fastq.gz	Fastqsanger.gz
	SRR22351303.fastq.gz	Fastqsanger.gz
	SRR22351304.fastq.gz	Fastqsanger.gz
	SRR22351305.fastq.gz	Fastqsanger.gz

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Telomere-to-mitochondria signaling by ZBP1 mediates replicative crisis (RIP-Seq)

Project description:Telomere-to-mitochondria signaling by ZBP1 mediates replicative crisis (RIP-Seq)

| PRJNA903483 | ENA

Telomere-to-mitochondria signaling by ZBP1 mediates replicative crisis (RNA-Seq)

Project description:Telomere-to-mitochondria signaling by ZBP1 mediates replicative crisis (RNA-Seq)

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Telomere-to-mitochondria signaling by ZBP1 mediates replicative crisis (RIP-Seq)

Project description:Interaction between ZBP1 and TERRA-derived RNA fragments

2022-12-12 | GSE218394 | GEO

Telomere-to-mitochondria signaling by ZBP1 mediates replicative crisis (RNA-Seq)

Project description:Transcriptional response to telomere shortening or dysfunction

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Telomere-to-mitochondria signalling by ZBP1 mediates replicative crisis.

Project description:Cancers arise through the accumulation of genetic and epigenetic alterations that enable cells to evade telomere-based proliferative barriers and achieve immortality. One such barrier is replicative crisis-an autophagy-dependent program that eliminates checkpoint-deficient cells with unstable telomeres and other cancer-relevant chromosomal aberrations1,2. However, little is known about the molecular events that regulate the onset of this important tumour-suppressive barrier. Here we identified the innate immune sensor Z-DNA binding protein 1 (ZBP1) as a regulator of the crisis program. A crisis-associated isoform of ZBP1 is induced by the cGAS-STING DNA-sensing pathway, but reaches full activation only when associated with telomeric-repeat-containing RNA (TERRA) transcripts that are synthesized from dysfunctional telomeres. TERRA-bound ZBP1 oligomerizes into filaments on the outer mitochondrial membrane of a subset of mitochondria, where it activates the innate immune adapter protein mitochondrial antiviral-signalling protein (MAVS). We propose that these oligomerization properties of ZBP1 serve as a signal amplification mechanism, where few TERRA-ZBP1 interactions are sufficient to launch a detrimental MAVS-dependent interferon response. Our study reveals a mechanism for telomere-mediated tumour suppression, whereby dysfunctional telomeres activate innate immune responses through mitochondrial TERRA-ZBP1 complexes to eliminate cells destined for neoplastic transformation.

| S-EPMC9946831 | biostudies-literature

Telomere-to-mitochondria signaling by ZBP1 mediates replicative crisis

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

2022-12-12 | GSE218396 | GEO

Illumina HiSeq next -generation sequencing of telomere fusion amplicons purified from crisis-stage MCR5HPVE6E7 and TALEN-transfected HCT116 cell lines at 48 and 120 hours post-transfection.

Project description:We sequenced and characterised inter-chromosomal and intra-chromosomal telomere fusions amplified from crisis-stage MCR5HPVE6E7 fibroblasts and DNA repair-compromised HCT116 cell lines nucleofected with plasmids encoding TALEN pairs to induce targeted cleavage at the 17p telomere.

2016-02-24 | E-MTAB-3811 | biostudies-arrayexpress

Alleviation of telomere dysfunction and mitochondria defects of telomerase deficient somatic cells by reprogramming

Project description:Somatic cell nuclear transfer (SCNT) and induced pluripotent stem cells (iPSCs) represent two major approaches for somatic cell reprogramming. However, little attention has been paid to the ability of these two strategies in rejuvenating cells from donors with aging associated syndrome. Here, we utilized telomerase deficient (Terc-/-) mice to probe this question. SCNT-derived embryonic stem cells (ntESCs) and iPSCs were successfully derived from second generation (G2) and third generation (G3) of Terc-/- mice, and ntESCs showed better differentiation potential and self-renewal ability. Telomeres lengthened extensively in cloned embryos while remained or slightly increased in the process of iPSCs induction. Furthermore, G3 ntESCs exhibited improvement of telomere capping function as evidenced by decreased signal free ends and chromosome end-to-end fusion events. In contrast, there was a further decline of telomere capping function in G3 iPSCs. In addition to telomere dysfunction, mitochondria function was severely impaired in G3 iPSCs as evidenced by oxygen consumption rate (OCR) decline, reactive oxygen species (ROS) accumulation and dramatically increased mitochondria genome mutations while these deficiencies were greatly mitigated in G3 ntESCs. Our data proved the principle that SCNT-mediated reprogramming appears more superior than transcription factors induced reprogramming in terms of the resetting of telomere quality and mitochondria function, and thus, providing valuable information for further improvement of transcription factors mediated reprogramming. We compared the gene expression profile of G3 Terc-/- ntES and G3 Terc-/- iPS. Three biological repeats were included for each cell line.

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Chromatin modifiers and recombination factors promote a telomere fold-back structure, that is lost during replicative senescence

Project description:Telomeres have the ability to adopt a lariat conformation and hence, engage in long and short distance intra-chromosome interactions. Budding yeast telomeres were proposed to fold back into subtelomeric regions, but a robust assay to quantitatively characterize this structure has been lacking. Therefore, it is not well understood how the interactions between telomeres and non-telomeric regions are established and regulated. We employ a telomere chromosome conformation capture (Telo-3C)approach to directly analyze telomere folding and its maintenance in S. cerevisiae. We identify the histone modifiers Sir2, Sin3 and Set2 as critical regulators for telomere folding, which suggests that a distinct telomeric chromatin environment is a major requirement for the folding of yeast telomeres. We demonstrate that telomeres are not folded when cells enter replicative senescence, which occurs independently of short telomere length. Indeed, Sir2, Sin3 and Set2 protein levels are decreased during senescence and their absence may thereby prevent telomere folding. Additionally, we show that the homologous recombination machinery, including the Rad51 and Rad52 proteins, as well as the checkpoint component Rad53 are essential for establishing the telomere fold-back structure. This study outlines a method to interrogate telomere-subtelomere interactions at a single unmodified yeast telomere. Using this method, we provide insights into how the spatial arrangement of the chromosome end structure is established and demonstrate that telomere folding is compromised throughout replicative senescence.

2020-11-20 | PXD021085 | Pride

Expression data from ZBP1-expression and ZBP1 nonexpression breast tumors.

Project description:ZBP1/IMP1 is an mRNA binding protein that post-transcriptionally regulates the expression of a handful mRNAs, implicated in maintaining cell polarity and adhesion. We have previously shown that ZBP1 was able to inhibit proliferation and invasiveness of breast carcinoma cells in vitro. In the current study, we utilized orthotopic breast fat pad xenografts to further investigate the ZBP1-mediated functions in breast tumorigenesis and metastasis in vivo. We used microarrays to identify important gene for breast tumor growth and metastasis in response to ZBP1 expression Total RNA was extracted from breast tumor generated from ZBP1-expression and ZBP1-nonexpression MDA231 cells and used for hybridization on Affymetrix microarrays. We sought to obtain gene expression profiles from the individual tumors and identify what genes are up-regulated or down-regulated in the presence of ZBP1. The microarray experiments and data analysis were performed in 'Gene Company Limited' in Senzheng, China. G-10 and G-13, Tumors generated from MDA231/GFP cells; I-5 and I-6, tumors generated from MDA231/ZBP1-GFP cells.

2014-10-24 | E-GEOD-62638 | biostudies-arrayexpress

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