Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Profiling Drosophila third instar larval eye discs with disruptions in Hippo and Rbf pathways by 10X single-cell RNA-Sequencing

ABSTRACT: We performed single-cell RNA-sequencing experiments to understand how the Rbf and Hippo pathways collaborate to maintain cell identity. Drosophila melanogaster photoreceptor neurons with dual mutation in Rbf[120a] and wts[x1] specify normally before abruptly dedifferentiating. We performed scRNA-Seq on w1118, Rbf[120a] single mutant, wts[x1] single mutant, and Rbf[120a] wts[x1] double mutant tissues to better understand the dedifferentiation phenotype. We identified transcriptional changes that were unique to double mutant tissue. We then validated these experiments using a novel dedifferentiation model expressing constitutively active yki[S111A,S168A,S250A] in Rbf[120a] mutant tissue using the GMR-GAL4 driver. We performed single-cell experiments on eye tissues expressing yki[S111A,S168A,S250A] in Rbf wildtype and mutant backgrounds, as well as tissues co-expressing Hth and yki. We then analyzed these experiments to determine the dedifferentiation transcriptional program.

ORGANISM(S): Drosophila melanogaster

PROVIDER: GSE217380 | GEO | 2023/08/04

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Hippo signaling instructs ectopic but not normal organ growth [Drosophila YkiHyper]

Project description:In order to study how ectopic Yki drives tissue overgrowth in Drosophila imaginal discs, we overexpressed the constitutively active Yki3SA and deleted wts in clones of cells in the entire eye-antennal imaginal disc, as well as specifically in eye disc proper cells using Optix-Gal4. Using the MARCM system allowed us to compare the effects of Yki3SA overexpression in wild-type and sd mutant clones.

2022-11-19 | GSE211458 | GEO

Genome-wide analysis of Yki and Sd localization in imaginal disks of Drosophila eye by ChIP Seq

Project description:Throughout Metazoa, developmental processes are controlled by a surprisingly limited number of conserved signaling pathways. Precisely how these signaling cassettes were assembled in early animal evolution remains poorly understood, as do the molecular transitions that potentiated the acquisition of their myriad developmental functions. Here we analyze the molecular evolution of the proto-oncogene YAP/Yorkie, a key effector of the Hippo signaling pathway that controls organ size in both Drosophila and mammals. Based on heterologous functional analysis of evolutionarily distant Yap/Yorkie orthologs, we demonstrate that a structurally distinct interaction interface between Yap/Yorkie and its partner TEAD/Scalloped became fixed in the eumetazoan common ancestor. We then combine transcriptional profiling of tissues expressing phylogenetically diverse forms of Yap/Yorkie with ChIP-seq validation in order to identify a common downstream gene expression program underlying the control of tissue growth in Drosophila. Intriguingly, a subset of the newly-identified Yorkie target genes are also induced by Yap in mammalian tissues, thus revealing a conserved Yap-dependent gene expression signature likely to mediate organ size control throughout bilaterian animals. Combined, these experiments provide new mechanistic insights while revealing the ancient evolutionary history of Hippo signaling. We sought to determine Yki and Sd target genes in Drosophila by immunoprecipitation of Yki, sd and RNA polymerase II. Chromatin immunoprecipitation of Yki, sd, and RNA polymerase II from eye disks was performed.

2014-03-01 | E-GEOD-54601 | biostudies-arrayexpress

Yorkie and Bonus protein interactome-Hippo pathway and Bonus control developmental cell fate decisions in the Drosophila eye

Project description:To identify novel regulators of the Hippo pathway, we performed affinity purification-mass spectrometry (AP-MS) using Drosophila embryos overexpressing Yki-EGFP with a ubiquitous driver da-GAL4, as well as cultured S2 cells expressing Yki-SBP. We identified the core Hippo pathway components, multiple Hippo pathway regulators and functional groups, and several putative Yki interactors including Bonus (Bon). To identify additional cofactors that are recruited by Bon, we performed AP-MS using Bon-SBP expressed in Drosophila S2 cells. Further genetic tests revealed the involvement of Bon interactors, HDAC1, Su(var)2-10, and Hrb27C, in the Drosophila eye specification that is regulated by the Yki-Bon complex.

2023-01-17 | PXD027934 | Pride

Single-cell RNA-seq profiling of Drosophila melanogaster Rbf mutant third instar eye discs

Project description:Wandering third instar larvae were dissected where the eye disc was separated from the antenna and brain using WT and Rbf mutants. The tissues were dissociated into single cells and captured using Drop-seq. Single cell libraries were then generated from each cell and finally sequenced.

2018-09-27 | E-MTAB-7194 | biostudies-arrayexpress

Microarray based gene expression comparison between wild type and yap-1(ys38) C. elegans embyos

Project description:Although multiple determinants for establishing polarity in membranes of epithelial cells have been identified, the mechanism for maintaining the apicobasal polarity is not fully understood. Here, we show that the conserved Hippo kinase pathway plays a role in the maintenance of apicobasal polarity in the developing intestine of Caenorhabditis elegans. We screened suppressors of the mutation in wts-1, the gene encoding the LATS kinase homolog, whose deficiency leads to the disturbance of the apicobasal polarity of the intestinal cells and the eventual death of organisms. Multiple alleles of yap-1 and egl-44, each encoding the worm homologs of YAP/Yki and TEAD/Sd, respectively, were identified as suppressors. WTS-1 directly bound to YAP-1 and inhibited its nuclear accumulation in intestinal cells. We also found that NFM-1, the worm homolog of NF2/Merlin, functioned in the same genetic pathway as WTS-1 to regulate YAP-1 for maintaining cellular polarity. The transcriptome analysis using microarray identified several target candidates of the YAP-1-EGL-44 complex including TAT-2, encoding a putative P-type ATPase. In summary, we have delineated the conserved Hippo pathway in worms consisting of NFM-1-WTS-1-YAP-1-EGL-44 and prove that the proper regulation of YAP-1 by upstream NFM-1 and WTS-1 is esssential for the maintenance of apicobasal membrane identities of the growing intestine

2019-07-02 | GSE133667 | GEO

In vivo reprogramming drives dedifferentiation and enhances liver regeneration

Project description:Mammalian tissues have a limited regenerative capacity. Previous studies showed that dedifferentiation contributes to tissue regeneration in non-mammalian vertebrate species such as zebrafish and newt. However, dedifferentiation is rarely observed in mammalian tissues even in the neonatal stage and therefore artificial induction of dedifferentiation might enhance regeneration in mammalian tissues. Here we demonstrate that short-term expression of Yamanaka 4 factors (4F) induces dedifferentiation and proliferation in the liver by using lineage-traceable, hepatocyte-specific 4F inducible mouse model. Global transcriptome analysis shows that 4F expression transiently reduces the expression of hepatic-lineage markers and induces the expression of a large set of proliferative markers and epigenetic modifiers along with global epigenetic changes as assessed by DNA-accessibility analysis. More importantly, lineage-tracing experiments showed that 4F-expressing hepatocytes acquire liver stem/progenitor cell markers, suggesting that 4F induces partial reprogramming. Moreover, 4F enhances MyoD-mediated transdifferentiation in the liver, suggesting that 4F endows hepatocytes with plasticity. Lastly, 4F expression attenuated liver injury associated with more proliferative capacity and better survival rate, indicating that 4F enhances liver regeneration. Taken together, these results demonstrate that liver-specific 4F expression induces dedifferentiation and promotes liver regeneration.

2022-04-27 | GSE144600 | GEO

A Novel Tumor suppressor network in squamous malignancies

Project description:The specific ablation of Rb1 gene in stratified epithelia (RbF/F;K14cre) promotes proliferation and altered differentiation but is insufficient to produce spontaneous tumors. The pRb relative, p107, compensates some of the functions of pRb in these tissues, however RbF/F;K14cre;p107-/- mice die postnatally. Acute pRb loss in stratified epithelia, using an inducible mouse model (RbF/F;K14creERTM), shows that p107 exerts specific tumor suppressor functions in its absence. After simultaneous absence of pRb and p107, p53 transcriptional function is impaired and Pten expression is reduced. All mutant mice develop spontaneous squamous tumors carcinomas rapidly. Gene expression analysis of mouse tumors, besides supporting the impaired p53 function and the susceptibility to Akt/mTOR inhibitors, also revealed significant overlap with human squamous carcinomas. Thus, RbF/F;K14creERTM;p107-/- may constitute a new mouse model for these malignancies. Collectively, these data demonstrate the existence of a previously unreported functional connection between pRb, Pten and p53 tumor suppressors, through p107, of a particular relevance in squamous tumor development.

2012-12-21 | GSE38257 | GEO

A Novel Tumor suppressor network in squamous malignancies

2012-12-21 | E-GEOD-38257 | biostudies-arrayexpress

Expression data from Control and Yorkie overexpression pupal eye discs

Project description:To probe mechanistic determinants of Yki function in mitochondrial biogenesis, we conducted a genome-wide microarray experiment, and specifically compared expression patterns of genes from control (GMR gal4) and Yorkie over-expressing (GMR gal4; UAS yki) pupal eye discs.

2011-12-20 | GSE26700 | GEO

Genome-wide analysis of Yki and Sd localization in imaginal disks of Drosophila eye by ChIP Seq

2014-03-01 | GSE54601 | 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