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Regulatory RNA Apela Is a Component of a Negative Feedback Loop Regulating p53-Mediated Apoptosis in Embryonic Stem Cells (II)

ABSTRACT: The goal is to identify regulatory RNAs that regulate the p53 signaling pathway in embryonic stem (ES) cells.

ORGANISM(S): Mus musculus

PROVIDER: GSE60843 | GEO | 2015/06/05

SECONDARY ACCESSION(S): PRJNA259654

REPOSITORIES: GEO

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Regulatory RNA Apela Is a Component of a Negative Feedback Loop Regulating p53-Mediated Apoptosis in Embryonic Stem Cells (II)

Project description:The goal is to identify regulatory RNAs that regulate the p53 signaling pathway in embryonic stem (ES) cells. p53+/+ mES cells and p53-/- mES cells were untreated or treated with 0.5 uM Adriamycin for 8 hours. Total RNA was extracted and subject to RNAseq.

2015-06-05 | E-GEOD-60843 | biostudies-arrayexpress

Regulatory RNA Apela Is a Component of a Negative Feedback Loop Regulating p53-Mediated Apoptosis in Embryonic Stem Cells (I)

Project description:p53-repressed transcripts have recently been shown to play important roles in various biological processes, such as stem cell differentiation and cancer. We identified a transcript named Apela that is repressed by p53 and highly expressed in mouse ES cells. To see which transcripts are affected by Apela knockdown, we performed gene expression microarray using Affymetrix Gene ST 1.0 array. Two short hairpin RNAs (shRNAs) targeting Apela were used to decrease the RNA levels of Apela to about 20% of the control (a shRNA target luciferase, shLuc). We designed two lentivirus-based shRNAs against Apela and used shRNA against luciferase as a control. Lentiviruses were made and used to transduced mouse ES cells. For each shRNA, three repeats were done.

2015-06-05 | E-GEOD-54355 | biostudies-arrayexpress

Regulatory RNA Apela Is a Component of a Negative Feedback Loop Regulating p53-Mediated Apoptosis in Embryonic Stem Cells (I)

2015-06-05 | GSE54355 | GEO

Regulatory RNA Apela Is a Component of a Negative Feedback Loop Regulating p53-Mediated Apoptosis in Embryonic Stem Cells (III)

Project description:The goal is to identify RNAs that bind to Hnrnpl (hnRNP L) using RNA immunoprecipitation (RIP) assay. p53+/+ mES cells and p53-/- mES cells were untreated or treated with 0.5 uM Adriamycin for 8 hours. RNA immunoprecipitation was performed using Hnrnpl antibody (Bethyl, Cat#: A311-423A). Total RNA was extracted and subject to RNAseq.

2015-06-05 | E-GEOD-62378 | biostudies-arrayexpress

Regulatory RNA Apela Is a Component of a Negative Feedback Loop Regulating p53-Mediated Apoptosis in Embryonic Stem Cells

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

2015-06-05 | GSE65491 | GEO

An Apela RNA-Containing Negative Feedback Loop Regulates p53-Mediated Apoptosis in Embryonic Stem Cells.

Project description:Maintaining genomic integrity is of paramount importance to embryonic stem cells (ESCs), as mutations are readily propagated to daughter cells. ESCs display hypersensitivity to DNA damage-induced apoptosis (DIA) to prevent such propagation, although the molecular mechanisms underlying this apoptotic response are unclear. Here, we report that the regulatory RNA Apela positively regulates p53-mediated DIA. Apela is highly expressed in mouse ESCs and is repressed by p53 activation, and Apela depletion compromises p53-dependent DIA. Although Apela contains a coding region, this coding ability is dispensable for Apela's role in p53-mediated DIA. Instead, Apela functions as a regulatory RNA and interacts with hnRNPL, which prevents the mitochondrial localization and activation of p53. Together, these results describe a tri-element negative feedback loop composed of p53, Apela, and hnRNPL that regulates p53-mediated DIA, and they further demonstrate that regulatory RNAs add a layer of complexity to the apoptotic response of ESCs after DNA damage.

| S-EPMC4458197 | biostudies-literature

Regulatory RNA Apela Is a Component of a Negative Feedback Loop Regulating p53-Mediated Apoptosis in Embryonic Stem Cells (III)

Project description:The goal is to identify RNAs that bind to Hnrnpl (hnRNP L) using RNA immunoprecipitation (RIP) assay.

2015-06-05 | GSE62378 | GEO

Corp Regulates P53 in Drosophila melanogaster via a Negative Feedback Loop.

Project description:The tumor suppressor P53 is a critical mediator of the apoptotic response to DNA double-strand breaks through the transcriptional activation of pro-apoptotic genes. This mechanism is evolutionarily conserved from mammals to lower invertebrates, including Drosophila melanogaster. P53 also transcriptionally induces its primary negative regulator, Mdm2, which has not been found in Drosophila. In this study we identified the Drosophila gene companion of reaper (corp) as a gene whose overexpression promotes survival of cells with DNA damage in the soma but reduces their survival in the germline. These disparate effects are shared by p53 mutants, suggesting that Corp may be a negative regulator of P53. Confirming this supposition, we found that corp negatively regulates P53 protein level. It has been previously shown that P53 transcriptionally activates corp; thus, Corp produces a negative feedback loop on P53. We further found that Drosophila Corp shares a protein motif with vertebrate Mdm2 in a region that mediates the Mdm2:P53 physical interaction. In Corp, this motif mediates physical interaction with Drosophila P53. Our findings implicate Corp as a functional analog of vertebrate Mdm2 in flies.

| S-EPMC4521751 | biostudies-literature

A p53/lnc-Ip53 Negative Feedback Loop Regulates Tumor Growth and Chemoresistance.

Project description:Acetylation is a critical mechanism to modulate tumor-suppressive activity of p53, but the causative roles of long non-coding RNAs (lncRNAs) in p53 acetylation and their biological significance remain unexplored. Here, lncRNA LOC100294145 is discovered to be transactivated by p53 and is thus designated as lnc-Ip53 for lncRNA induced by p53. Furthermore, lnc-Ip53 impedes p53 acetylation by interacting with histone deacetylase 1 (HDAC1) and E1A binding protein p300 (p300) to prevent HDAC1 degradation and attenuate p300 activity, resulting in abrogation of p53 activity and subsequent cell proliferation and apoptosis resistance. Mouse xenograft models reveal that lnc-Ip53 promotes tumor growth and chemoresistance in vivo, which is attenuated by an HDAC inhibitor. Silencing lnc-Ip53 inhibits the growth of xenografts with wild-type p53, but not those expressing acetylation-resistant p53. Consistently, lnc-Ip53 is upregulated in multiple cancer types, including hepatocellular carcinoma (HCC). High levels of lnc-Ip53 is associated with low levels of acetylated p53 in human HCC and mouse xenografts, and is also correlated with poor survival of HCC patients. These findings identify a novel p53/lnc-Ip53 negative feedback loop in cells and indicate that abnormal upregulation of lnc-Ip53 represents an important mechanism to inhibit p53 acetylation/activity and thereby promote tumor growth and chemoresistance, which may be exploited for anticancer therapy.

| S-EPMC7610266 | biostudies-literature

Identification of a mechanochemical checkpoint and negative feedback loop regulating branching morphogenesis.

Project description:Cleft formation is the initial step in submandibular salivary gland (SMG) branching morphogenesis, and may result from localized actomyosin-mediated cellular contraction. Since ROCK regulates cytoskeletal contraction, we investigated the effects of ROCK inhibition on mouse SMG ex vivo organ cultures. Pharmacological inhibitors of ROCK, isoform-specific ROCK I but not ROCK II siRNAs, as well as inhibitors of myosin II activity stalled clefts at initiation. This finding implies the existence of a mechanochemical checkpoint regulating the transition of initiated clefts into progression-competent clefts. Downstream of the checkpoint, clefts are rendered competent through localized assembly of fibronectin promoted by ROCK I/myosin II. Cleft progression is primarily mediated by ROCK I/myosin II-stimulated cell proliferation with a contribution from cellular contraction. Furthermore, we demonstrate that FN assembly itself promotes epithelial proliferation and cleft progression in a ROCK-dependent manner. ROCK also stimulates a proliferation-independent negative feedback loop to prevent further cleft initiations. These results reveal that cleft initiation and progression are two physically and biochemically distinct processes.

| S-EPMC3183484 | biostudies-literature

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