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Maintenance of cell fate by the Polycomb Group gene Sex combs extra enables a partial epithelial mesenchymal transition in Drosophila (Pc dataset)

ABSTRACT: Maintenance of cell fate by the Polycomb Group gene Sex combs extra enables a partial epithelial mesenchymal transition in Drosophila (Pc dataset)

PROVIDER: PRJNA644505 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12161887.fastq.gz	Fastqsanger.gz
	SRR12161888.fastq.gz	Fastqsanger.gz
	SRR12161889.fastq.gz	Fastqsanger.gz
	SRR12161890.fastq.gz	Fastqsanger.gz
	SRR12161891.fastq.gz	Fastqsanger.gz

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Similar Datasets

Maintenance of cell fate by the Polycomb Group gene Sex combs extra enables a partial epithelial mesenchymal transition in Drosophila (Pc dataset)

Project description:Epigenetic silencing by Polycomb group (PcG) complexes can promote epithelial-mesenchymal transition (EMT) and stemness and is associated with malignancy of solid cancers. Here we report a role for Drosophila PcG repression in a partial EMT event that occurs during wing disc eversion, an early event during metamorphosis. In a screen for EMT genes required for eversion we identified the PcG genes Sex combs extra (Sce) and Sex combs midleg (Scm). Depletion of Sce or Scm resulted in internalised wings and thoracic clefts, and loss of Sce inhibited the EMT of the peripodial epithelium and basement membrane breakdown, ex vivo. Targeted DamID (TaDa) using Dam-Pol II showed that Sce knockdown caused a genomic transcriptional response consistent with maintenance of an epithelial fate. Surprisingly only 17 genes were significantly upregulated in Sce-depleted cells, including Abd-B, abd-A, caudal, and nubbin. Each of these loci were enriched for Dam-Pc binding. Of the four genes, only Abd-B was robustly upregulated in cells lacking Sce expression. RNAi knockdown of all four genes could partly suppress the Sce RNAi eversion phenotype, though Abd-B had the strongest effect. Our results suggest that in the absence of continued PcG repression peripodial cells express genes such as Abd-B which regulate epithelial state and thereby disrupt eversion. Our results emphasise the important role that PcG suppression can play in maintaining cell states required for morphogenetic events throughout development and suggest that PcG repression of Hox genes may affect epithelial traits that could contribute to metastasis.

2020-12-31 | GSE153904 | GEO

Maintenance of cell fate by the Polycomb Group gene Sex combs extra enables a partial epithelial mesenchymal transition in Drosophila (Pol2 dataset)

2020-12-31 | GSE153903 | GEO

Maintenance of cell fate by the Polycomb Group gene Sex combs extra enables a partial epithelial mesenchymal transition in Drosophila (Pol2 dataset)

Project description:Maintenance of cell fate by the Polycomb Group gene Sex combs extra enables a partial epithelial mesenchymal transition in Drosophila (Pol2 dataset)

| PRJNA644504 | ENA

Maintenance of cell fate by the Polycomb Group gene Sex combs extra enables a partial epithelial mesenchymal transition in Drosophila

Project description:Maintenance of cell fate by the Polycomb Group gene Sex combs extra enables a partial epithelial mesenchymal transition in Drosophila

| PRJNA644501 | ENA

Maintenance of Cell Fate by the Polycomb Group Gene Sex Combs Extra Enables a Partial Epithelial Mesenchymal Transition in <i>Drosophila</i>.

Project description:Epigenetic silencing by Polycomb group (PcG) complexes can promote epithelial-mesenchymal transition (EMT) and stemness and is associated with malignancy of solid cancers. Here we report a role for Drosophila PcG repression in a partial EMT event that occurs during wing disc eversion, an early event during metamorphosis. In a screen for genes required for eversion we identified the PcG genes S ex combs extra (Sce) and S ex combs midleg ( Scm ) Depletion of Sce or Scm resulted in internalized wings and thoracic clefts, and loss of Sce inhibited the EMT of the peripodial epithelium and basement membrane breakdown, ex vivo. Targeted DamID (TaDa) using Dam-Pol II showed that Sce knockdown caused a genomic transcriptional response consistent with a shift toward a more stable epithelial fate. Surprisingly only 17 genes were significantly upregulated in Sce-depleted cells, including Abd-B, abd-A, caudal, and nub bin Each of these loci were enriched for Dam-Pc binding. Of the four genes, only Abd-B was robustly upregulated in cells lacking Sce expression. RNAi knockdown of all four genes could partly suppress the Sce RNAi eversion phenotype, though Abd-B had the strongest effect. Our results suggest that in the absence of continued PcG repression peripodial cells express genes such as Abd-B, which promote epithelial state and thereby disrupt eversion. Our results emphasize the important role that PcG suppression can play in maintaining cell states required for morphogenetic events throughout development and suggest that PcG repression of Hox genes may affect epithelial traits that could contribute to metastasis.

| S-EPMC7718746 | biostudies-literature

Morganella morganii subsp. morganii PC strain:PC

Project description:Morganella morganii subsp. morganii PC strain:PC Genome sequencing

| PRJNA175476 | ENA

Identification of new regulators of the three dimensional Polycomb organization by a microscopy-based genome-wide RNAi screen

Project description:Polycomb group (PcG) proteins dynamically define cellular identities through epigenetic repression of key developmental genes. PcG target gene repression can be stabilized through the interaction in the nucleus at PcG foci. Here, we report the results of a high-resolution microscopy genome-wide RNAi screen that identifies 129 genes that regulate the nuclear organization of Pc foci. Candidate genes include PcG components and chromatin factors, as well as many novel protein-modifying enzymes, including components of the SUMOylation pathway. In the absence of SUMO Pc foci coagulate into larger aggregates. Conversely, loss of function of the SUMO peptidase velo disperses Pc foci. Moreover, SUMO and velo colocalize with PcG proteins at PREs and Pc SUMOylation affects its chromatin targeting, suggesting that the dynamic regulation of Pc SUMOylation regulates PcG-mediated silencing by modulating the kinetics of Pc binding to chromatin as well as its ability to form Polycomb foci. ChIP-Seq mapping of Polycomb (PC), SUMO and Velo on Drosophila Melanogaster

2014-04-03 | E-GEOD-55303 | biostudies-arrayexpress

Multiple hierarchies of Polycomb targeting to Drosophila genome (Part 3)

Project description:Polycomb group (PcG) proteins are critical epigenetic regulators of development. Here we compared genomic distribution of Polycomb (Pc) protein in cultured Drosophila cells lacking Su(z)12 protein to that of the wild type.

2016-09-15 | GSE83247 | GEO

Mapping of Polycomb binding in Drosophila larval brain tissue using DamID

Project description:We made Polycomb (PC) and histone H3 lysine 27 trimethylation (H3K27me3) chromatin binding maps in central brain tissue from 3rd instar larvae, allowing us to make a direct comparison to our 4C data (http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE23166). Our results demonstrate that our PC and H3K27me3 maps are highly similar, and fit with previously identified hallmarks of PcG-bound chromatin, namely: PC and H3K27me3 co-occur in the genome as large contiguous domains that largely repress transcription of the underlying genes, which encode important regulators of development. Keywords: Genome binding/occupancy profiling by genome tiling array DamID experiments for Polycomb were performed in Drosophila larval brain tissue. Samples were hybridized to 380k NimbleGen arrays with 300 bp probe spacing.

2011-12-31 | E-GEOD-23298 | biostudies-arrayexpress

Arabidopsis Polycomb Repressive Complex 2 binding sites contain putative GAGA factor binding motifs within coding regions of genes

Project description:Background. Polycomb Repressive Complex 2 (PRC2) is an essential regulator of gene expression that maintains genes in a repressed state by marking chromatin with trimethylated Histone H3 lysine 27 (H3K27me3). In Arabidopsis, loss of PRC2 function leads to pleiotropic effects on growth and development thought to be due to ectopic expression of seed and embryo-specific genes. While there is some understanding of the mechanisms by which specific genes are targeted by PRC2 in animal systems, it is still not clear how PRC2 is recruited to specific regions of plant genomes.Results. We used ChIP-seq to determine the genome-wide distribution of hemagglutinin (HA)-tagged FERTLIZATION INDEPENDENT ENDOSPERM (FIE-HA), the Extra Sex Combs homolog protein present in all Arabidopsis PRC2 complexes. We found that the FIE-HA binding sites co-locate with a subset of the H3K27me3 sites in the genome and the associated genes were more likely to be de-repressed in mutants of PRC2 components. The FIE-HA binding sites are enriched for three sequence motifs including a putative GAGA factor binding site that is also found in Drosophila Polycomb Response Elements (PREs).Conclusions. Our results suggest that PRC2 binding sites in plant genomes share some sequence features with Drosophila PREs. However, RNA was extracted from intermediate phenotype siFIE plants, clf-7 swn-28 and Col using Qiagen Plant RNeasy mini kit. For each sample, three pools of 10-12 plants were used. The siFIE plants were analysed for FIE mRNA by RT-qPCR; the maximum level of FIE mRNA was found to be 10% of wildtype.

2013-09-01 | E-GEOD-48857 | biostudies-arrayexpress

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