Drosophila melanogaster
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: E-GEOD-28728
PROVIDER: PRJNA140535 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Genome wide localization of Kumgang, dMi-2, and Aly in Drosophila melanogaster testes were evaluated by ChIP-Seq in wild-type and kmg knock down testes. / Title: Blocking promiscuous activation at cryptic promoters directs cell type–specific gene expression / Abstract: To selectively express cell type–specific transcripts during development, it is critical to maintain genes required for other lineages in a silent state. Here, we show in the Drosophila male germline stem cell lineage that a spermatocyte-specific zinc finger protein, Kumgang (Kmg), working with the chromatin remodeler dMi-2 prevents transcription of genes normally expressed only in somatic lineages. By blocking transcription from normally cryptic promoters, Kmg restricts activation by Aly, a component of the testis-meiotic arrest complex, to transcripts for male germ cell differentiation. Our results suggest that as new regions of the genome become open for transcription during terminal differentiation, blocking the action of a promiscuous activator on cryptic promoters is a critical mechanism for specifying precise gene activation.
2017-05-18 | GSE89381 | GEO
Project description:Tissue homeostasis requires long-term lineage fidelity of somatic stem cells. Whether and how age-related changes in somatic stem cells impact the faithful execution of lineage decisions remains largely unknown. Here, we address this question using genome-wide chromatin accessibility and transcriptome analysis as well as single cell RNA-seq to explore stem cell intrinsic changes in the aging Drosophila intestine. These studies indicate that in stem cells of old flies, promoters of Polycomb (Pc) target genes become differentially accessible, resulting in the increased expression of enteroendocrine (EE) cell specification genes. Consistently, we find age related changes in the composition of the EE progenitor cell population in aging intestines, as well as a significant increase in the proportion of EE-specified ISCs and progenitors in aging flies. We further confirm that Pc-mediated chromatin regulation is a critical determinant of EE cell specification in the Drosophila intestine. Pc is required to maintain expression of stem cell genes while ensuring repression of differentiation and specification genes. Our results identify Pc group proteins as central regulators of lineage identity in the intestinal epithelium and highlight the impact of age-related decline in chromatin regulation on tissue homeostasis.
2021-04-02 | GSE157794 | GEO
Project description:Tissue homeostasis requires long-term lineage fidelity of somatic stem cells. Whether and how age-related changes in somatic stem cells impact the faithful execution of lineage decisions remains largely unknown. Here, we address this question using genome-wide chromatin accessibility and transcriptome analysis as well as single cell RNA-seq to explore stem cell intrinsic changes in the aging Drosophila intestine. These studies indicate that in stem cells of old flies, promoters of Polycomb (Pc) target genes become differentially accessible, resulting in the increased expression of enteroendocrine (EE) cell specification genes. Consistently, we find age related changes in the composition of the EE progenitor cell population in aging intestines, as well as a significant increase in the proportion of EE-specified ISCs and progenitors in aging flies. We further confirm that Pc-mediated chromatin regulation is a critical determinant of EE cell specification in the Drosophila intestine. Pc is required to maintain expression of stem cell genes while ensuring repression of differentiation and specification genes. Our results identify Pc group proteins as central regulators of lineage identity in the intestinal epithelium and highlight the impact of age-related decline in chromatin regulation on tissue homeostasis.
2021-04-02 | GSE157776 | GEO
Project description:Tissue homeostasis requires long-term lineage fidelity of somatic stem cells. Whether and how age-related changes in somatic stem cells impact the faithful execution of lineage decisions remains largely unknown. Here, we address this question using genome-wide chromatin accessibility and transcriptome analysis as well as single cell RNA-seq to explore stem cell intrinsic changes in the aging Drosophila intestine. These studies indicate that in stem cells of old flies, promoters of Polycomb (Pc) target genes become differentially accessible, resulting in the increased expression of enteroendocrine (EE) cell specification genes. Consistently, we find age related changes in the composition of the EE progenitor cell population in aging intestines, as well as a significant increase in the proportion of EE-specified ISCs and progenitors in aging flies. We further confirm that Pc-mediated chromatin regulation is a critical determinant of EE cell specification in the Drosophila intestine. Pc is required to maintain expression of stem cell genes while ensuring repression of differentiation and specification genes. Our results identify Pc group proteins as central regulators of lineage identity in the intestinal epithelium and highlight the impact of age-related decline in chromatin regulation on tissue homeostasis.
2021-04-02 | GSE157775 | GEO
Project description:Active Promoters give rise to false positive 'Phantom Peaks' in ChIP-Seq experiments
| PRJNA279510 | ENA
Project description:Genome-wide localization of exosome components to active promoters and chromatin insulators in Drosophila
| PRJNA178575 | ENA
Project description:Cellular differentiation entails loss of pluripotency and parallel gain of lineage-specific and ultimately cell-type specific characteristics. Using a murine system that progresses from stem cells to lineage-committed progenitors and further to terminally differentiated neurons we analyzed two repressive epigenetic pathways: DNA methylation and Polycomb-mediated methylation of histone H3 (H3K27me3). We show that several hundred promoters become DNA methylated in lineage-committed progenitor cells. Targets are selected for pluripotency and germline-specific genes, suggesting a role for DNA methylation in stabilizing loss of pluripotency already at the progenitor state. Conversely, we detect loss and acquisition of H3K27me3 at novel targets at both progenitor and terminal state. Surprisingly, many neuron-specific genes that are poised to be activated upon terminal differentiation become Polycomb targets only in progenitor cells. Moreover, promoters marked by H3K27me3 in stem cells frequently become DNA methylated during differentiation, suggesting context-dependent crosstalk between Polycomb and DNA methylation. This data suggest a new model how de novo DNA methylation and dynamic switches in Polycomb targets restrict pluripotency and define the developmental potential of progenitor cells. Keywords: MeDIP-chip, ChIP-chip, neuronal differentiation time-course MeDIP-chip and ChIP-chip experiments were performed with at least two independnet biological replicates. For each condition hybridizations include a dye-swap experiment.
2008-06-04 | E-GEOD-11489 | biostudies-arrayexpress
Project description:Stonewalling Drosophila stem cell differentiation by epigenetic controls
| PRJNA99355 | ENA
Project description:Peroxisome elevation induces stem cell differentiation and intestinal epithelial repair
| PRJNA563469 | ENA
Project description:Cellular differentiation entails loss of pluripotency and parallel gain of lineage-specific and ultimately cell-type specific characteristics. Using a murine system that progresses from stem cells to lineage-committed progenitors and further to terminally differentiated neurons we analyzed two repressive epigenetic pathways: DNA methylation and Polycomb-mediated methylation of histone H3 (H3K27me3). We show that several hundred promoters become DNA methylated in lineage-committed progenitor cells. Targets are selected for pluripotency and germline-specific genes, suggesting a role for DNA methylation in stabilizing loss of pluripotency already at the progenitor state. Conversely, we detect loss and acquisition of H3K27me3 at novel targets at both progenitor and terminal state. Surprisingly, many neuron-specific genes that are poised to be activated upon terminal differentiation become Polycomb targets only in progenitor cells. Moreover, promoters marked by H3K27me3 in stem cells frequently become DNA methylated during differentiation, suggesting context-dependent crosstalk between Polycomb and DNA methylation. This data suggest a new model how de novo DNA methylation and dynamic switches in Polycomb targets restrict pluripotency and define the developmental potential of progenitor cells. Keywords: MeDIP-chip, ChIP-chip, neuronal differentiation time-course
2008-06-04 | GSE11489 | GEO