Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Studies of autophagy pathway during submergence in Arabidopsis thaliana

ABSTRACT: Autophagy involves massive degradation of intracellular components and functions as a conserved system that helps cells to adapt to adverse conditions. In Arabidopsis thaliana, submergence induces the transcription of autophagy-related (ATG) genes and the formation of autophagosomes. To study the role of autophagy during submergence, we performed transcriptome analysis with atg5, an autophagy-defective mutant, under submergence conditions. Our data showed that submergence changed the expression profile of DEG in the atg5 versus wild-type.

ORGANISM(S): Arabidopsis thaliana

PROVIDER: GSE184340 | GEO | 2021/09/20

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Autophagy and alternative NF-kappaB inhibition by RNAi against RELB, ATG5 or ULK1 in A549 human cancer cells

Project description:In order to understand the contribution of autophagy and alternative NF-kappaB signalling to transcriptional output in A549 lung cancer cells, RNAi was used to knockdown the expression of core autophagy genes (ATG5, ULK1) or the key subunit of alternative NF-kappaB RELB. Seven samples were prepared for each biological replicate; two sequence independent non-targeting control siRNAs were transfected as a negative control. Three sequence independent siRNAs targeting the core autophagy machinery were transfected (ATG5 si, ATG5 si(2), ULK1 si). N.B. ATG5 si(2) only partially ablates Atg5 protein expression whereas ATG si has greater efficacy. Two sequence independent siRNAs targeting RELB were transfected (RELB si, RELB si(2) ). Three independent biological replicates of all conditions were obtained, by performance of the experiment on different days.

2015-09-18 | E-GEOD-73158 | biostudies-arrayexpress

Studies of autophagy pathway during submergence in Arabidopsis thaliana

Project description:Studies of autophagy pathway during submergence in Arabidopsis thaliana

| PRJNA764178 | ENA

Unique position of ATG5 in the atg8ylation cascade provides a switch between autophagy and secretion

Project description:ATG5 is a part of the E3 ligase directing lipidation of ATG8 proteins (mATG8s), a process central to membrane atg8ylation and its downstream homeostatic manifestations, including canonical autophagy, with impact on health. Genetic ablation of ATG5 in myeloid cells causes mortality in murine models of tuberculosis. Paradoxically, this in vivo phenotype is specific to ATG5 and does not apply to other ATGs. Here we show that absence of ATG5 but not of other components of canonical autophagy, promotes lysosomal exocytosis, secretion of extracellular vesicles, and in neutrophils their excessive degranulation. This is due to lysosomal disrepair in ATG5 knockout cells and sequestration of ESCRT proteins by an alternative ATG conjugation complex. These findings explain the unique nature of ATG5 in host-protective role in murine experimental models of tuberculosis, and emphasize the significance of the branching aspects of the atg8ylation conjugation cascade beyond the canonical autophagy.

| MSV000090348 | MassIVE

Transcriptional profiling of autophagy proficient and compromised cell lines, determined by expression levels of Atg5

Project description:Autophagy is activated in pancreatic ductal adenocarcinoma (PDAC) and is currently being considered a promising therapeutic target in clinical trials. PDAC is a highly lethal disease with incidence rate equalling mortality rate. Main reasons for PDAC lethality are late-stage diagnosis, high agressiveness and metastatic rate, lack of effective treatments as well as specific diagnostic markers. Here we show that varying levels of the Autophagy related gene 5 (Atg5) determine pancreatic tumor formation and malignancy. While homozygous deletion of Atg5 blocks tumor progression in an in vivo model of PDAC, heterozygous deletion increases tumor aggressiveness and metastasis. Further analyses reveal that monoallelic loss of Atg5 affects mitochondrial homeostasis, changes intracellular calcium oscillations, heightens extracellular cathepsin activities , and promotes a pro-tumorigenic inflammatory microenvironment collectively enhancing tumor cell migration, invasion, and metastasis. Future treatments should take into account that variations in the autophagy pathway may have opposing effects on pancreatic tumor load, especially considering the multitude of autophagy inhibitors currently tested in clinical trials.

2018-10-15 | E-MTAB-6275 | biostudies-arrayexpress

Response to Bruton's tyrosine kinase inhibitors in aggressive lymphomas linked to chronic selective autophagy

Project description:We uncovered an autophagic pathway regulating survival in ABC DLBCL upon BTK inhibition using genome wide CRISPR screening. To investigate the mechanism of action of this unique form of autophagy, we performed RNA-seq on TMD8 cells knocked out for various ATG genes that either showed resistance to BTK inhibitors (ATG9A, ATG101, ATG14, RB1CC1, WIPI2), those that did not (ATG5, ATG7, ULK1 and 2 DKO, or non-targetingcontrol), or TMD8 cells knocked out for the known NF-kB negative regulator TNFAIP3. Cells were treated for 24 hours with the BTK inhibitor, acalabrutinib, and gene expression signatures were calculated from normalized RNA-seq reads. We found NF-kB gene expression signatures to be downregulated in control cells upon BTK inhibition, but not in ATG KO cells conferring BTK inhibitor resistance.

2024-01-30 | GSE227465 | GEO

Autophagy promotes plant survival by maintaining nutrient cycling and energy supply during submergence

Project description:Autophagy promotes plant survival by maintaining nutrient cycling and energy supply during submergence

2023-05-10 | PXD042109 | iProX

Identification Atg5-related microRNAs involved in the regulation of tumor formation

Project description:Autophagy plays an important role in physiology and tumorigenesis. We and others have demonstrated that Ha-ras overexpression induces autophagy in NIH3T3 cells. Autophagic machinery is regulated by a family of autophagy associated genes (Atg). The inducible Ha-ras oncogene was introduced into mouse embryo fibroblast Atg5 wild type [MEF-Atg5(+/+)] and Atg5 knock-out [MEF-Atg5(-/-)] cells and the stable cell lines MR and M5R were established, respectively. Our results showed that M5R cell induced larger tumor formation compared with MR cells while these two cell lines were subcutaneously injected into SCID mice under Ha-ras overexpression conditions. It indicates that Atg5 is involved in the suppression of Ras-related tumor formation. MicroRNA (miRNA), approximately 22 nucleotide of non-coding RNA, regulates transcription and translation of the target genes and is involved in cell differentiation and tumorigenesis. A miRNA microarray (932 probes) screening was conducted to identify the autophagy-tumorigenesis-related miRNAs. Among the significant genes, miR-224 was highly expressed in autophagy deficient cell and it induced tumors. Overexpression miR-224 enhanced the activity of migration and invasion in vitro and tumor formation in vivo. In conclusion, this is the first report to demonstrate that autophagy suppresses tumor formation through down-regulation of microRNA in this case miR-224. MR and M5R cell lines were treated with IPTG for 48 hr. In addition, these cell lines were subcutaneously injected into mice to induce tumor formation. The RNA samples were extracted from above cell lines and tumors. In this research, BEL/ITRI 15K V1.0 miRNA microarray chips were used to evaluate the miRNA expression profile.

2012-06-25 | E-GEOD-38911 | biostudies-arrayexpress

Autophagy is essential for cardiac morphogenesis during vertebrate development

Project description:This study examined the effects of genetic knockdown of autophagy genes on vertebrate cardiac development We performed microarray studies comparing the hearts of control zebrafish embryos to the hearts of embryos with decreased expression of the autophagy genes atg5, becn1 or atg7. The results provide insight into the role of autophagy in developmental morphogenesis. Hearts were purified from 3 day-old zebrafish embryos injected with control or autophagy gene-specific morpholino oligonucleotides. RNA was prepared from all samples and hybridized to zebrafish-specific Affymetricx arrays.

2014-03-01 | E-GEOD-51541 | biostudies-arrayexpress

Autophagy Suppresses CD8+ T cell Anti-tumour Immunity

Project description:Here we demonstrate that inactivation of the essential autophagy genes, Atg5, Atg14, or Atg16L1 results in tumour rejection. Despite a significant reduction in the total number of CD8+ tumour infiltrating lymphocytes (TILs), loss of Atg5 causes a profound shift toward IFNg and TNF producing effector memory cells. Consistent with this, adoptive transfer with Atg5-/- T cells promotes tumour control. Mechanistically, CD8+ T cells lacking autophagy exhibit enhanced glucose metabolism resulting in global changes in histone trimethylation and increased transcriptional activation of effector target genes. Restricting glucose is sufficient to suppress autophagy-dependent increases in effector function and reverse alterations in histone trimethylation. These findings identify autophagy as a cell-autonomous negative regulator of CD8+ T cell anti-tumour immunity with implications on T cell-based immunotherapy.

2019-04-09 | GSE117757 | GEO

Autophagy-Mediated Degradation of Integumentary Tapetum Is Critical for Embryo Pattern Formation

Project description:To investigate molecular links and underlying mechanisms between autophagy in the integumentary tapetum and embryo pattern formation, we isolated embryos from wild-type plants, atg5 mutants, and atg5 mutants expressing proTPE8:ATG5-GFP for RNA-sequencing.

2024-02-20 | GSE248624 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data