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Global transcriptional profiling of HEK293 cells transfected with ATFs, mouse embryonic fibroblasts, and mouse iPS cells derived with artificial transcription factors

ABSTRACT: Global transcriptional profiling of HEK293 cells transfected with ATFs, mouse embryonic fibroblasts, and mouse iPS cells derived with artificial transcription factors

OTHER RELATED OMICS DATASETS IN: GSE89219GSE89221

PROVIDER: PRJNA350708 | ENA |

REPOSITORIES: ENA

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Global transcriptional profiling of HEK293 cells transfected with ATFs, mouse embryonic fibroblasts, and mouse iPS cells derived with artificial transcription factors

Project description:We tested various architectures of artificial transcription factors (ATFs) in HEK293 cells to test the contribution of the interaction domain, nuclear localization domain, size of DNA-binding domain, and activation domain. Then we made a genome-scale ATF library and tested it in reprogramming mouse embryonic fibroblasts to induced pluripotent stem (iPS) cells. Three combinations of ATFs (C2, C3, and C4) could induce pluripotency when expressed with Sox2, Klf4, and c-Myc. We harvested polyadenylated RNAs from 11 cell types derived with different sets of factors. The transcriptional profiles of ATF-induced iPS cells are similar to that of iPS cells induced with Oct4, Sox2, Klf4, and c-Myc and mouse embryonic stem cells, exhibiting up-regulation of pluripotency markers and down-regulation of fibroblast markers. Comparisons of cells undergoing reprogramming at an intermediate stage before becoming fully reprogrammed suggest that ATFs activate a different set of genes than the set activated by Oct4. This study provides a proof-of-principle that a gene-activating ATF library can be used to identify cell fate-defining transcriptional networks in an unbiased manner.

2016-12-05 | GSE89219 | GEO

ATFS-1 regulates a broad protective transcriptional program

Project description:We previously identified a number of genes which were differentially expressed during mitochondrial stress in an ATFS-1-dependent manner using an atfs-1 loss-of-function mutant allele . To complement the findings from our previous microarray, we compared the transcript profiles from wild-type and atfs-1(et18) gain-of-function worms (which have constitutively active ATFS-1) in the absence of mitochondrial stress. We used microarrays to identify genes regulated by ATFS-1 using a gain-of-function allele of atfs-1.

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ATFS-1 mediates a protective transcription program during mitochondrial stress

Project description: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 RNA samples were prepared from wild-type(wt) and atfs-1(tm4525)(mutant) worms fed either control(RNAi) or spg-7(RNAi). Worms were synchronized by bleaching, raised in liquid culture and harvested at the L4 stage. Control is denoted as C and spg-7 treatment is denoted T. Each experiment was performed in triplicate indicated as 1,2 and 3.

2012-07-11 | E-GEOD-38196 | biostudies-arrayexpress

To identify ATFS-1 target genes during mitochondrial stress

Project description:To better understand genome coordination and OXPHOS recovery during mitochondrial dysfunction, we examined ATFS-1, a transcription factor that regulates mitochondria-to nuclear communication during the mitochondrial UPR, via ChIP-sequencing. Wildtype worms treated spg-7(RNAi) are analyzed in the presence and absence of ATFS-1 antibody to identify ATFS-1 targets. Individual samples were analyzed. Wildtype worms treated spg-7(RNAi) in the absence of antibody is used as a control.

2015-03-03 | E-GEOD-63803 | biostudies-arrayexpress

Comparison of WT to atfs-1(null) & WT to atfs-1(et18) in C. elegans by deep sequencing

Project description:Comparison of gene change in the atfs-1 (null) to WT. Comparison of gene change in the atfs-1 (et18) to WT.

2020-12-02 | GSE114951 | GEO

ATFS-1 mediates a protective transcription program during mitochondrial stress

2012-07-12 | GSE38196 | GEO

RNAseq profiling of Aire and Ctr-transfected HEK293 cells

Project description:Aire-sensitive genes exhibit short 3'UTR transcript isoform preference in Aire and Ctr-transfected HEK293 cells

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

Project description: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.

2018-11-21 | GSE110984 | GEO

ChIP-seq of H3K27ac, H3K9me3, and HA tag for ATFs on MEF-derived cells

Project description:We tested a genome-scale artificial transcription factor (ATF) library in reprogramming mouse embryonic fibroblasts to induced pluripotent stem (iPS) cells. Three combinations of ATFs (C2, C3, and C4) could induce pluripotency when expressed with Sox2, Klf4, and c-Myc. The transcriptional profiles of ATF-induced iPS cells are similar to that of iPS cells induced with Oct4, Sox2, Klf4, and c-Myc and mouse embryonic stem cells, exhibiting up-regulation of pluripotency markers and down-regulation of fibroblast markers. We performed ChIP-seq on the active histone mark H3K27ac and the repressive histone mark H3K9me3 in C2+SKM iPS cells, C3+SKM iPS cells, in Oct4+SKM to validate the total transcriptome results. In addition, the ATFs from C2 were chromatin immunoprecipitated to determine where they are bound in the genome at an intermediate stage before being fully reprogrammed to iPS cells. This study provides a proof-of-principle that a gene-activating ATF library can be used to identify cell fate-defining transcriptional networks in an unbiased manner.

2016-12-05 | GSE89220 | GEO

V-ATPase/TORC1-mediated ATFS-1 translation directs mitochondrial UPR activation in C. elegans

Project description:To adapt mitochondrial function to the ever-changing intra- and extra-cellular environment, multiple mitochondrial stress response (MSR) pathways, including the mitochondrial unfolded protein response (UPRmt), have evolved. However, how the mitochondrial stress signal is sensed and relayed to UPRmt transcription factors, such as ATFS-1 in Caenorhabditis elegans, remains largely unknown. Here, we show that a panel of vacuolar H+-ATPase (v-ATPase) subunits and the target of rapamycin complex 1 (TORC1) activity are essential for the cytosolic relay of mitochondrial stress to ATFS-1, and for the induction of the UPRmt. Mechanistically, mitochondrial stress stimulates v-ATPase/Rheb-dependent TORC1 activation, subsequently promoting ATFS-1 translation. Increased translation of ATFS-1 upon mitochondrial stress furthermore relies on a set of ribosomal components, but is independent of GCN-2/PEK-1 signaling. Finally, the v-ATPase and ribosomal subunits are required for mitochondrial surveillance and mitochondrial stress-induced longevity. These results reveal a v-ATPase-TORC1-ATFS-1 signaling pathway that links mitochondrial stress to the UPRmt through intimate crosstalks between multiple organelles.

2022-09-23 | GSE179517 | GEO

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