Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

TRNA sequencing Drosophila wildtype and ectopic neuroblast brains

ABSTRACT: tRNA quantification of neuron-biased and neuroblast-biased Drosophila larval brains

ORGANISM(S): Drosophila melanogaster

PROVIDER: GSE276447 | GEO | 2024/09/05

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Neuroblast-specific open chromatin allows the temporal transcription factor, Hunchback, to bind neuroblast-specific loci

Project description:Integration of spatial and temporal identity during Drosophila neurogenesis is due to spatial factors generating neuroblast-specific chromatin thereby biasing subsequent temporal transcription factor binding and producing neuroblast-specific neurons.

2019-01-25 | GSE123272 | GEO

Single-cell RNA-seq analysis of Drosophila neuroblast tumors

Project description:Inactivation of prospero in Drosophila neuroblasts during larval stages induces unlimited neuroblast amplification leading to tumors that persist growing in adults. Tumors present in the ventral nerve cord of adult flies were dissected, dissociated and GFP-labelled tumor neuroblasts were isolated by FACS. 10000 neuroblasts were then processed for single-cell RNA-seq analysis. Single Cell RNA sequencing library were generated using the 10x Genomics Chromium Platform and sequenced on the Illumina Nextseq 500. eLife 2019;8:e50375 DOI: 10.7554/eLife.50375

2019-10-10 | GSE114986 | GEO

Acsl mutants repress neuroblast development

Project description:We found Acsl mutants have deficient neuroblast development. Further experiment confirmed that genes related to cell cycle and pluripotency were supressed in Acsl mutants.

2019-07-01 | GSE118275 | GEO

Notch targets stem-cell and temporal-programming genes to orchestrate neuroblast tumours

Project description:Notch signalling is involved in a multitude of developmental decisions and its aberrant activation is linked to many diseases, including cancers. One such example is the neural stem cell tumours that arise from constitutive Notch activity in Drosophila neuroblasts. To investigate how hyper-activation of Notch in larval neuroblasts leads to tumours, we combined results from profiling the upregulated mRNAs and mapping the regions bound by Su(H) (the core Notch pathway transcription factor ). This identified 127 putative direct Notch targets that were up-regulated in the hyperplastic tissue. These genes were highly enriched for transcription factors (TFs) and overlapped significantly with a previously identified regulatory programme dependent on the proneural transcription factor Asense. Included were genes associated with the neuroblast maintenance and self-renewal programme that we validated as Notch regulated in vivo. A second category contained so-called temporal transcription factors, which are involved in neuroblast progression. Normally expressed in specific time windows, several temporal transcription factors were ectopically expressed in the stem cell tumours, suggesting that Notch had reprogrammed the normal temporal hierarchy. Indeed, the Notch-induced hyperplasia was reduced by mutations affecting two of the temporal factors which, conversely, were sufficient to induce mild hyperplasia on their own. Altogether the results demonstrate that Notch induces neural stem cell tumors by promoting the expression of genes that contribute to stem cell identity and by reprogramming expression of temporal factors that regulate maturity.

2016-10-18 | E-MTAB-3561 | biostudies-arrayexpress

Acsl mutants repress neuroblast development

Project description:Acsl mutants repress neuroblast development

| PRJNA485050 | ENA

Single-cell RNA-seq of Drosophila neuroblast tumors induced by the knockdown of prospero, E(z) and trx

Project description:COMPASS and Polycomb complexes are antagonistic chromatin complexes that are frequently inactivated in cancers, but how their inactivation affects the cellular hierarchy, composition and growth of tumors is unclear. Such characteristics can be systematically investigated in Drosophila neuroblast tumors in which cooption of temporal patterning induces a developmental hierarchy that confers cancer stem cell (CSC) properties to a subset of neuroblasts retaining an early larval temporal identity. Here, using single-cell transcriptomics, we reveal that the trithorax/MLL1/2-COMPASS-like complex guides the developmental trajectory at the top of the tumor hierarchy. Consequently, trithorax inactivation drives larval-to-embryonic temporal reversion and the dramatic expansion of CSCs that remain locked in a spectrum of early temporal states. Surprisingly, this phenotype is amplified by concomitant inactivation of Polycomb Repressive Complex 2 genes, unleashing tumor growth. This study exemplifies how inactivation of specific COMPASS and Polycomb complexes cooperates to impair tumor hierarchies and induce CSC plasticity and heterogeneity.

2021-08-31 | GSE179154 | GEO

Neuroblast-specific open chromatin allows the temporal transcription factor, Hunchback, to bind neuroblast-specific loci

Project description:Neuroblast-specific open chromatin allows the temporal transcription factor, Hunchback, to bind neuroblast-specific loci

| PRJNA507995 | ENA

Quantification of tRNA-derived fragments in Arabidopsis and rice

Project description:Quantification of tRNA-derived fragments in Arabidopsis and rice

| PRJNA512644 | ENA

meRIP_seq m6A mapping

Project description:meRIP_seq and Input total RNA_seq in neuroblast-biases brains, neuron-biased brains, and Mettl3 null brains

2022-09-26 | GSE214058 | GEO

Myc and the Tip60 chromatin remodeling complex control neuroblast maintenance and polarity in Drosophila

Project description:Stem cells establish cortical polarity and divide asymmetrically to simultaneously maintain themselves and generate differentiating offspring cells. Several chromatin modifiers have been identified as stemness factors in mammalian pluripotent stem cells, but whether these factors control stem cell polarity and asymmetric division has not been investigated so far. We addressed this question in Drosophila neural stem cells called neuroblasts. We identified the Tip60 chromatin remodeling complex and its interaction partner Myc to regulate target genes required for neuroblast maintenance. Knockdown of members of this complex results in loss of cortical polarity, symmetric neuroblast division and premature differentiation through nuclear entry of the transcription factor Prospero. We found that aPKC is the key target gene of Myc and the Tip60 complex subunit Domino regulating neuroblast polarity. Our transcriptome analysis further showed that Domino regulates the expression of mitotic spindle genes which were identified before as direct Myc targets. Our findings reveal an evolutionarily conserved functional link between Myc, the Tip60 complex and the molecular network controlling cell polarity and asymmetric cell division.

2018-07-06 | PXD009939 | Pride

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

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