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

ABSTRACT: Transcriptional response to telomere shortening or dysfunction

ORGANISM(S): Homo sapiens

PROVIDER: GSE218395 | GEO | 2022/12/12

REPOSITORIES: GEO

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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

Telomere-to-mitochondria signaling by ZBP1 mediates replicative crisis

Project description:Telomere-to-mitochondria signaling by ZBP1 mediates replicative crisis

| PRJNA903482 | ENA

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 (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 (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)

| PRJNA903485 | ENA

Telomere dysfunction and fusion during the progression of chronic lymphocytic leukaemia: evidence for a telomere crisis

Project description:We performed single-molecule telomere length and telomere fusion analysis in patients at different stages of chronic lymphocytic leukaemia (CLL). Our work identified the shortest telomeres ever recorded in primary human tissue reinforcing the concept that there is significant cell division in CLL. Furthermore, we provide direct evidence that critical telomere shortening, dysfunction and fusion contribute to disease progression. The frequency of short telomeres and fusion events increased with advanced disease, but importantly these were also found in a subset of early-stage patient samples indicating that these events can precede disease progression. Sequence analysis of fusion events isolated from individuals with the shortest telomeres revealed limited numbers of repeats at the breakpoint, sub-telomeric deletion and microhomology. Array-CGH analysis of individuals displaying evidence of telomere dysfunction revealed large-scale genomic rearrangements that were concentrated in the telomeric regions; this was not observed in samples with longer telomeres. Array CGH was undertaken on six individuals (five CLL stage C and one stage A) that displayed evidence of telomere dysfunction, and four (three CLL stage A and one stage B) that displayed longer and apparently stable telomeres.

2010-05-28 | E-GEOD-22016 | biostudies-arrayexpress

Telomere dysfunction and fusion during the progression of chronic lymphocytic leukaemia: evidence for a telomere crisis

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Length-independent telomere damage drives cardiomyocyte senescence

Project description:Ageing is the biggest risk factor to cardiovascular health and is associated with increased incidence of cardiovascular disease. Cellular senescence, a process driven in part by telomere shortening has been implicated in age-related cardiac dysfunction. However, the role of cellular senescence and its underlying mechanisms in slowly dividing/post-mitotic cardiomyocytes is not understood.

2019-02-06 | GSE95822 | GEO

The Human Telomeric Proteome During Telomere Replication

Project description:Telomere shortening can cause detrimental diseases and contribute to aging. It occurs due to the end replication problem in cells lacking telomerase. In addition, recent evidence revealed that telomere shortening can be attributed to difficulties of the semi-conservative DNA replication machinery to replicate through the bulk of telomeric DNA repeats. To investigate telomere replication in a comprehensive manner, we developed QTIP-iPOND, which enables purification of the proteins that associate with telomeres during their replication. We identify in addition to the core replisome a large number of proteins that specifically associate with telomere replication forks and validate their importance.

2021-11-03 | PXD018712 | Pride

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