Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

53 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Translational control of autophagy by Orb in the Drosophila germline [mature]

ABSTRACT: Drosophila Orb, the homologue of vertebrate CPEB is a key translational regulator involved in oocyte polarity and maturation through poly(A) tail elongation of specific mRNAs. orb has also an essential function during early oogenesis which has not been addressed at the molecular level. Here, we show that orb prevents cell death during early oogenesis, thus allowing oogenesis to progress. It does so through the repression of autophagy, by directly repressing, together with the CCR4 deadenylase, the translation of Autophagy-specific gene 12 (Atg12) mRNA. Autophagy and cell death observed in orb mutant ovaries are reduced by decreasing Atg12 or other Atg mRNA levels. These results reveal a role of Orb in translational repression and identify autophagy as an essential pathway regulated by Orb during early oogenesis. Importantly, they also establish translational regulation as a major mode of control of autophagy, a key process in cell homeostasis in response to environmental cues. Orb RIP-chip vs mock IP on ovaries from mature 3-5 day old females.

ORGANISM(S): Drosophila melanogaster

SUBMITTER: Simonelig Martine

PROVIDER: E-GEOD-74475 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Translational control of autophagy by Orb in the Drosophila germline [early]

Project description:Drosophila Orb, the homologue of vertebrate CPEB is a key translational regulator involved in oocyte polarity and maturation through poly(A) tail elongation of specific mRNAs. orb has also an essential function during early oogenesis which has not been addressed at the molecular level. Here, we show that orb prevents cell death during early oogenesis, thus allowing oogenesis to progress. It does so through the repression of autophagy, by directly repressing, together with the CCR4 deadenylase, the translation of Autophagy-specific gene 12 (Atg12) mRNA. Autophagy and cell death observed in orb mutant ovaries are reduced by decreasing Atg12 or other Atg mRNA levels. These results reveal a role of Orb in translational repression and identify autophagy as an essential pathway regulated by Orb during early oogenesis. Importantly, they also establish translational regulation as a major mode of control of autophagy, a key process in cell homeostasis in response to environmental cues. Orb RIP-chip vs mock IP on ovaries from newly eclosed females.

2016-07-03 | E-GEOD-74474 | biostudies-arrayexpress

Translational control of autophagy by Orb in the Drosophila germline [mature]

2016-01-01 | GSE74475 | GEO

Translational control of autophagy by Orb in the Drosophila germline [early]

2016-01-01 | GSE74474 | GEO

Translational control of autophagy by Orb in the Drosophila germline

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2016-07-03 | E-GEOD-74476 | biostudies-arrayexpress

Cpeb4-mediated Translational Regulatory Circuitry Controls Terminal Erythroid Differentiation

Project description:Erythropoiesis is essential to mammals and is regulated at multiple steps by both extracellular and intracellular factors. Many transcriptional regulatory networks in erythroid differentiation have been well characterized. However, our understanding of post-transcriptional regulatory circuitries in this developmental process is still limited. Using genomic approaches, we identified a sequence-specific RNA-binding protein, Cpeb4, which is dramatically induced in terminal erythroid differentiation (TED) by two erythroid important transcription factors, Gata1/Tal1. Cpeb4 belongs to the cytoplasmic polyadenylation element binding (CPEB) protein family that regulates translation of target mRNAs in early embryonic development, neuronal synapse, and cancer. Using primary mouse fetal liver erythroblasts, we found that Cpeb4 is required for terminal erythropoiesis by repressing the translation of a set of mRNAs highly expressed in progenitor cells. This translational repression occurs by the interaction with a general translational initiation factor, eIF3. Interestingly, Cpeb4 also binds its own mRNA and represses its translation, thus forming a negative regulatory circuitry to limit Cpeb4 protein level. This mechanism ensures that the translation repressor, Cpeb4, does not interfere with the translation of other mRNAs in differentiating erythroblasts. Our study characterized a translational regulatorycircuitry that controls TED and revealed that Cpeb4 is required for somatic cell differentiation. We used microarray to identify mRNAs associated with Cpeb4 in mouse fetal liver erythroblasts. Cpeb4 associated mRNAs were isolated from mouse fetal liver erythroblasts using anti-Cpeb4 antibody for immunoprecipitation followed by RNA extraction. Then Affymetrix microarrays were used to identify and quantify the mRNAs associated with Cpeb4.

2015-12-09 | E-GEOD-57004 | biostudies-arrayexpress

Oogenesis in Solea senegalensis: various developmental stages

Project description:This SuperSeries is composed of the following subset Series: GSE17333: Oogenesis in Solea senegalensis: Vitellogenic versus mature ovaries GSE17334: Oogenesis in Solea senegalensis: vitellogenic versus atretic ovaries GSE17335: Oogenesis in Solea senegalensis: mature versus atretic ovaries GSE17336: Oogenesis in Solea senegalensis: Previtellogenic versus vitellogenic ovaries Refer to individual Series

2010-06-21 | E-GEOD-17337 | biostudies-arrayexpress

Relative Quantification of the Effect of Blood Meal Iron on Protein Expression in Mosquito Ovaries 24 h Post Feeding

Project description:Aedes aegypti [Linnaeus in Hasselquist (Diptera: Culicidae); yellow fever mosquito] transmits several viruses that infect millions of people each year including, Zika, dengue, yellow fever, chikungunya, and West Nile. Disease transmission occurs during blood feeding. Only the females blood feed as they require a bloodmeal for oogenesis. In the bloodmeal, females receive a substantial iron load in the forms of holo-transferrin and hemoglobin. We are interested in the effects of the iron in a bloodmeal on the expression of proteins during oogenesis. Our previous data showed that during digestion of a blood meal, the gut iron concentration decreases 10-fold, while that of the ovaries doubles from ingestion to 72 hours post feeding. Approximately 72 hours post feeding, eggs are laid with ~125 ng Fe each. We are interested in the effects of the blood meal iron on the expression of proteins detected in the ovaries during the early oogenesis, 24 hours post feeding, before eggs are laid. We have used tandem mass tag-labeling proteomics to quantify proteins expressed at this early stage following feeding of a controlled iron diet. Our findings provide the first quantitative report of differential ovary protein expression in early oogenesis in mosquitoes fed three different iron diets.

2022-03-26 | PXD028242 | Pride

Autophagy maintains metabolism and functional activity of a subset of aged hematopoietic stem cells [gene expression]

Project description:Autophagy is critical for protecting HSCs from metabolic stress. Here, we used a genetic approach to inactivate autophagy in adult HSCs by deleting the Atg12 gene. We show that loss of autophagy causes accumulation of mitochondria and an oxidative phosphorylation (OXPHOS)-activated metabolic state, which drives accelerated myeloid differentiation likely through epigenetic deregulations rather than transcriptional changes, and impairs HSC self-renewal activity and regenerative potential. To determine how loss of autophagy affects gene expression, we conducted microarray analysis of purified control and Atg12 conditional knockout HSCs.

2017-03-03 | GSE81719 | GEO

Autophagy maintains metabolism and functional activity of a subset of aged hematopoietic stem cells [RRBS]

Project description:Autophagy is critical for protecting HSCs from metabolic stress. Here, we used a genetic approach to inactivate autophagy in adult HSCs by deleting the Atg12 gene. We show that loss of autophagy causes accumulation of mitochondria and an oxidative phosphorylation (OXPHOS)-activated metabolic state, which drives accelerated myeloid differentiation likely through epigenetic deregulations rather than transcriptional changes, and impairs HSC self-renewal activity and regenerative potential. To determine how loss of autophagy affects DNA methylation, we conducted enhanced reduce representation bisulfite sequencing (ERRBS) of purified control and Atg12 conditional knockout HSCs.

2017-03-03 | GSE81720 | GEO

CPEB Deficiency Stimulates PTEN and Stat3 mRNA Translation and Induces Hepatic Insulin Resistance

Project description:Analysis of CPEB translational regulator target mRNAs

2011-05-01 | GSE28106 | GEO