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Links from GEO DataSets

Items: 20

1.

DVE-1_ChIP-seq and HDA-1_ChIP-seq of worms

(Submitter supplied) Mitochondria are important organelles, but their function is often challenged by toxic products of metabolism as well as by pathogen attack. The mitochondrial unfolded protein response (UPRmt) monitors mitochondrial function in general: it is responsible for buffering the mitochondrial protein folding environment, and controlling mitochondria-nuclear balance of the electron transport chain (ETC) components. more...
Organism:
Caenorhabditis elegans
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL25147
36 Samples
Download data: BED, TXT
Series
Accession:
GSE141042
ID:
200141042
2.

mRNA-seq of worms and the mitochondrial unfolded protein response (UPRmt)

(Submitter supplied) To cope with a challenging and unpredictable environment, living systems have evolved several organelle-specific stress responses, e.g. the cytosolic heat shock response (HSR), the endoplasmic reticulum unfolded protein response (UPRER) and the mitochondrial unfolded protein response (UPRmt). UPRmt monitors mitochondrial function and homeostasis in general. However, the mechanism of UPRmt remains largely unexplored. more...
Organism:
Caenorhabditis elegans
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18245
12 Samples
Download data: XLSX
Series
Accession:
GSE141041
ID:
200141041
3.

The transcriptional coactivator CBP/p300 is an evolutionarily conserved node that promotes longevity in response to mitochondrial stress [HepG2]

(Submitter supplied) Organisms respond to mitochondrial stress by activating multiple defense pathways including the mitochondrial unfolded protein response (UPRmt). However, how different layers of UPRmt regulators are orchestrated to transcriptionally activate the stress responses remains largely unknown. Here we identified CBP-1, the worm ortholog of the mammalian acetyltransferases CBP/p300, as an essential regulator for UPRmt activation, as well as for mitochondrial stress-induced immune response, amyloid-β aggregation reduction and lifespan extension in Caenorhabditis elegans. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL23227
12 Samples
Download data: XLSX
4.

The transcriptional coactivator CBP/p300 is an evolutionarily conserved node that promotes longevity in response to mitochondrial stress [ChIP-seq]

(Submitter supplied) Organisms respond to mitochondrial stress by activating multiple defense pathways including the mitochondrial unfolded protein response (UPRmt). However, how different layers of UPRmt regulators are orchestrated to transcriptionally activate the stress responses remains largely unknown. Here we identified CBP-1, the worm ortholog of the mammalian acetyltransferases CBP/p300, as an essential regulator for UPRmt activation, as well as for mitochondrial stress-induced immune response, amyloid-β aggregation reduction and lifespan extension in Caenorhabditis elegans. more...
Organism:
Caenorhabditis elegans
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL25145
6 Samples
Download data: XLSX
Series
Accession:
GSE148328
ID:
200148328
5.

The transcriptional coactivator CBP/p300 is an evolutionarily conserved node that promotes longevity in response to mitochondrial stress

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Caenorhabditis elegans; Mus musculus; Homo sapiens
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platforms:
GPL23227 GPL23479 GPL25145
57 Samples
Download data
Series
Accession:
GSE131616
ID:
200131616
6.

The transcriptional coactivator CBP/p300 is an evolutionarily conserved node that promotes longevity in response to mitochondrial stress [Mus musculus]

(Submitter supplied) Organisms respond to mitochondrial stress by activating multiple defense pathways including the mitochondrial unfolded protein response (UPRmt). However, how different layers of UPRmt regulators are orchestrated to transcriptionally activate the stress responses remains largely unknown. Here we identified CBP-1, the worm ortholog of the mammalian acetyltransferases CBP/p300, as an essential regulator for UPRmt activation, as well as for mitochondrial stress-induced immune response, amyloid-β aggregation reduction and lifespan extension in Caenorhabditis elegans. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL23479
12 Samples
Download data: XLSX
Series
Accession:
GSE131613
ID:
200131613
7.

The transcriptional coactivator CBP/p300 is an evolutionarily conserved node that promotes longevity in response to mitochondrial stress [C. elegans]

(Submitter supplied) Organisms respond to mitochondrial stress by activating multiple defense pathways including the mitochondrial unfolded protein response (UPRmt). However, how different layers of UPRmt regulators are orchestrated to transcriptionally activate the stress responses remains largely unknown. Here we identified CBP-1, the worm ortholog of the mammalian acetyltransferases CBP/p300, as an essential regulator for UPRmt activation, as well as for mitochondrial stress-induced immune response, amyloid-β aggregation reduction and lifespan extension in Caenorhabditis elegans. more...
Organism:
Caenorhabditis elegans
Type:
Expression profiling by high throughput sequencing
Platform:
GPL25145
27 Samples
Download data: XLSX
Series
Accession:
GSE131611
ID:
200131611
8.

Two Conserved Histone Demethylases Regulate Mitochondrial Stress-Induced Longevity

(Submitter supplied) Across eukaryotic species, mild mitochondrial stress can have beneficial effects on the lifespan of organisms. Mitochondrial dysfunction activates an unfolded protein response (UPRmt), a stress signaling mechanism designed to ensure mitochondrial homeostasis. Perturbation of mitochondria during larval development in C. elegans not only delays aging but also maintains UPRmt signaling, suggesting an epigenetic mechanism that modulates both longevity and mitochondrial proteostasis throughout life. more...
Organism:
Caenorhabditis elegans
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18245
15 Samples
Download data: TXT
Series
Accession:
GSE78990
ID:
200078990
9.

Mitochondrial stress induces chromatin reorganization to promote longevity and UPRmt

(Submitter supplied) Organisms respond to mitochondrial stress through the upregulation of an array of protective genes, often perpetuating an early response to metabolic dysfunction across a lifetime. We find that mitochondrial stress causes widespread changes in chromatin structure through histone H3K9 di-methylation marks traditionally associated with gene silencing. Mitochondrial stress response activation requires the di-methylation of histone H3K9 through the activity of the histone methyltransferase met-2 and the nuclear co-factor lin-65. more...
Organism:
Caenorhabditis elegans
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18245
18 Samples
Download data: TXT
Series
Accession:
GSE78252
ID:
200078252
10.

Polysome profiling and mRNA-seq to quantify translational gene regulation in dietary restricted C. elegans and in a long-lived daf-2:rsks-1 double mutant.

(Submitter supplied) Dietary restriction (DR) and loss of the genes rsks-1 and daf-2 increase longevity in C. elegans. Polysome profiling allows actively translated mRNA bound by multiple ribosomes to be isolated and compared to the total mRNA present. In this project, we differentiate transcriptional and translational changes in gene expression in C. elegans by combining polysome profiling and mRNA-sequencing. By comparing gene abundance between the two RNA pools, genes with altered translational regulation under DR and in the mutant can be identified.
Organism:
Caenorhabditis elegans
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13657
24 Samples
Download data: TXT
Series
Accession:
GSE119485
ID:
200119485
11.

Role of mitochondrial unfolded protein response transcription fatcor ATFS-1 in lifespan of long-lived mitochondrial mutants

(Submitter supplied) In this work, we examined the effect of the transcription factor ATFS-1 in the long lifespan of the nuo-6 mitochondrial mutant. We also examined the effect of the hypoxia transcription factor hif-1. We sequenced both atfs-1 deletion mutants and atfs-1 gain-of-function point mutants in which the mitochondrial localization sequence of ATFS-1 is disrupted. Note that sequencing batch 2 was previously uploaded as part of GSE93724.
Organism:
Caenorhabditis elegans
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19757
43 Samples
Download data: TXT
Series
Accession:
GSE110984
ID:
200110984
12.

The chromatin factors SET-26 and HCF-1 oppose the histone deacetylase HDA-1 in longevity and gene regulation in C. elegans

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Caenorhabditis elegans
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL19757
113 Samples
Download data
Series
Accession:
GSE224078
ID:
200224078
13.

The chromatin factors SET-26 and HCF-1 oppose the histone deacetylase HDA-1 in longevity and gene regulation in C. elegans [CUT&RUN]

(Submitter supplied) SET-26, HCF-1, and HDA-1 are highly conserved chromatin factors with key roles in development and aging. Here we present mechanistic insights into how these factors regulate gene expression and modulate longevity in C. elegans. We show that SET-26 and HCF-1 cooperate to regulate a common set of genes, and both antagonize the histone deacetylase HDA-1 to limit longevity. We propose a model in which SET-26 recruits HCF-1 to chromatin in somatic cells, where they stabilize each other at the promoters of a subset of genes, particularly mitochondrial function genes, and regulate their expression. more...
Organism:
Caenorhabditis elegans
Type:
Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL19757
83 Samples
Download data: BIGWIG, NARROWPEAK, TXT
Series
Accession:
GSE224076
ID:
200224076
14.

The chromatin factors SET-26 and HCF-1 oppose the histone deacetylase HDA-1 in longevity and gene regulation in C. elegans [RNA-Seq]

(Submitter supplied) SET-26, HCF-1, and HDA-1 are highly conserved chromatin factors with key roles in development and aging. Here we present mechanistic insights into how these factors regulate gene expression and modulate longevity in C. elegans. We show that SET-26 and HCF-1 cooperate to regulate a common set of genes, and both antagonize the histone deacetylase HDA-1 to limit longevity. We propose a model in which SET-26 recruits HCF-1 to chromatin in somatic cells, where they stabilize each other at the promoters of a subset of genes, particularly mitochondrial function genes, and regulate their expression. more...
Organism:
Caenorhabditis elegans
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19757
30 Samples
Download data: TXT
Series
Accession:
GSE224075
ID:
200224075
15.

ATFS-1 mediates a protective transcription program during mitochondrial stress

(Submitter supplied) ATFS-1 has been shown to regulate transcription of mitochondrial chaperone genes such as mtHsp70/hsp-6 and hsp-60 in response to mitocondrial stress. To identify the entire ATFS-1-mediated response, we compared the transcript profiles from wild-type and atfs-1(tm4525) worms raised in the absence and presence of mitochondrial stress. We used microarrays to identify genes regulated by ATFS-1 during mitochondrial stress
Organism:
Caenorhabditis elegans
Type:
Expression profiling by array
Dataset:
GDS4570
Platform:
GPL200
12 Samples
Download data: CEL, CHP
Series
Accession:
GSE38196
ID:
200038196
16.
Full record GDS4570

Mitochondrial stress effect on ATFS-1 mutants

Analysis of atfs-1 mutants raised on spg-7(RNAi) which induces mitochondrial stress (MS). ATFS-1 (activating transcription factor associated with stress-1) senses MS and communicates with the nucleus during the mitochondrial unfolded protein response. Results provide insight into the MS response.
Organism:
Caenorhabditis elegans
Type:
Expression profiling by array, count, 2 genotype/variation, 2 protocol sets
Platform:
GPL200
Series:
GSE38196
12 Samples
Download data: CEL, CHP
17.

Differential expression analysis of wildtype, atfs-1(tm4919) and zip-3(gk3164) mutant with next generation sequencing

(Submitter supplied) ZIP-3 has been shown to repress the mitochondrial-UPR response. To identify genes repressed by ZIP-3, we compared transcript profiles from wildtype, atfs-1(tm4919) and zip-3(gk3164) worms raised on control RNAi or spg-7 RNAi
Organism:
Caenorhabditis elegans
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24892
18 Samples
Download data: TXT
Series
Accession:
GSE113136
ID:
200113136
18.

 Differential expression analysis of wildtype and zip-3(gk3164) mutant with next generation sequencing

(Submitter supplied) ZIP-3 has been shown to repress the mitochondrial-UPR genes and immune response during P. aeruginosa infection. To identify genes repressed by ZIP-3, we compared transcript profiles from wildtype and zip-3(gk3164) worms raised on P. aeruginosa or E. coli.
Organism:
Caenorhabditis elegans
Type:
Expression profiling by high throughput sequencing
Platform:
GPL13657
12 Samples
Download data: TXT
Series
Accession:
GSE111325
ID:
200111325
19.

RNA-sequencing of C. elegans long-lived mutants eat-2, ife-2, osm-5 and glp-1

(Submitter supplied) Long-lived genetic mutants from different pathways of lifespan extension were used to determine the extent to which there are common downstream mediators of longevity. We have previously obtained RNA-sequencing data from other long-lived mutants including sod-2, clk-1, isp-1, nuo-6 and daf-2. Gene expression will be compared between these nine long-lived mutants.
Organism:
Caenorhabditis elegans
Type:
Expression profiling by high throughput sequencing
Platform:
GPL19757
36 Samples
Download data: CSV
Series
Accession:
GSE179825
ID:
200179825
20.

Expression data from C. elegans in the presence or absence of copper sulfate

(Submitter supplied) MAP kinases are integral to the mechanisms by which cells respond to a wide variety of environmental stresses. In Caenorhabditis elegans, the KGB-1 JNK signaling pathway regulates the response to heavy metal stress. The deletion mutants of this cascade show hypersensitivity to heavy metals like copper or cadmium. However, factors that function downstream of KGB-1 pathway are not well characterized. To understand how the KGB-1 pathway modulates gene activity and to define the physiological processes in which the heavy metal stress response may be involved, we used microarray to examine gene expression changes in wild-type and kgb-1 mutant animals subjected to heavy metal stress.
Organism:
Caenorhabditis elegans
Type:
Expression profiling by array
Dataset:
GDS4568
Platform:
GPL200
4 Samples
Download data: CEL, CHP
Series
Accession:
GSE42703
ID:
200042703
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