Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression of E93 provides an instructive cue to control dynamic enhancer activity and chromatin accessibility during development

ABSTRACT: How temporal cues combine with spatial inputs to control gene expression during development is poorly understood. Here, we test the hypothesis that the Drosophila transcription factor E93 controls temporal gene expression by regulating chromatin accessibility. Precocious expression of E93 early in wing development reveals that it can simultaneously activate and deactivate different target enhancers. Notably, the precocious patterns of enhancer activity resemble the wild-type patterns that occur later in development, suggesting that provision of E93 alters the competence of enhancers to respond to spatial cues. Genomic profiling reveals that precocious E93 expression is sufficient to regulate chromatin accessibility at a subset of its targets. These accessibility changes mimic those that normally occur later in development, indicating that precocious E93 accelerates the wild-type developmental program. Further, we find that target enhancers that do not respond to precocious E93 in early wings become responsive after a developmental transition, suggesting that parallel temporal pathways work alongside E93. These findings support a model wherein E93 expression functions as an instructive cue that defines a broad window of developmental time through control of chromatin accessibility.

ORGANISM(S): Drosophila melanogaster

PROVIDER: GSE141738 | GEO | 2020/02/25

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Chromatin remodeling and expression dynamics reveal conserved and species-specific regulation during mouse and chicken limb development [ATAC-seq]

Project description:Understanding the origin of morphological diversity across vertebrates is central to evolutionary developmental biology. cis-regulatory elements (CRE) such as enhancers and promoters interpret precise spatiotemporal cues to control and coordinate gene expression. To get insights into both conserved and species-specific variations during early limb patterning and outgrowth, we leverage genome-wide comprehensive assessment of chromatin accessibility and transcriptional changes during mouse forelimb and chicken wing bud development. Our analysis reveals temporal modulation of chromatin accessibility and expression as well as their temporal relationship during the progression of mouse forelimb and chicken wing bud development. Transcription factor binding site enrichment analysis and putative TF occupancy as inferred by integrating TF binding motifs and chromatin accessibility information reveal temporal TF-DNA interactions during forelimb/wing bud patterning. Finally, the integration of accessibility, expression, and TF binding site information allowed to identify candidate gene targets of HAND2 and GLI3 that include conserved as well as species-specific transcriptional regulator-gene interactions.

2021-07-31 | GSE164736 | GEO

Chromatin remodeling and expression dynamics reveal conserved and species-specific regulation during mouse and chicken limb development [RNA-seq]

2021-07-31 | GSE164737 | GEO

Hierarchical enhancers 1 confer the temporal and partially compensatory transcriptional regulation of Nkx2-5 during heart development

Project description:We comprehensively interrogate enhancers U1 and U2 in controlling Nkx2-5 transcription during heart development. Serial genomic deletions in mice reveal a functional hierarchy of U1 and U2 as evidenced by stage-dependent phenotypic variations. Specifically, U1 and U2 function redundantly to confer Nkx2-5 expression at early stages, but U2 instead of U1 supported its expression at later stages of heart chamber formation and maturation. Combined deletions markedly reduce Nkx2-5 dosage as early as E7.5, despite being largely reinstated two days later, displaying heart malformations with precocious differentiation of cardiac progenitors. Together, we propose a model that the temporal and partially compensatory regulatory function of two enhancers dictates a TF?s dosage and specificity during development.

2022-07-03 | GSE133760 | GEO

Hormone-dependent control of developmental timing through regulation of chromatin accessibility

Project description:We identify a temporal cascade of ecdysone-inducible transcription factor gene expression during Drosophila wing development. This temporal cascade corresponds with dynamic changes in chromatin accesibility during wing development. We hypothesized that these temporally regulated transcription factors may coordinate these dynamic open chromatin changes. To test this, we investigate the ecdysone-inducible transcription factor, E93, which we determine is required for coordinating transitions in developmental stage by regulating chromatin accesibility of cis-regulatory elements.

2017-06-06 | GSE97956 | GEO

Drosophila E93 promotes adult development and suppresses larval responses to ecdysone during metamorphosis

Project description:Pulses of the steroid hormone ecdysone act through transcriptional cascades to direct the major developmental transitions during the Drosophila life cycle. These include the prepupal ecdysone pulse, which occurs 10 hours after pupariation and triggers the onset of adult morphogenesis and larval tissue destruction. E93 encodes a transcription factor that is specifically induced by the prepupal pulse of ecdysone, supporting a model proposed by earlier work that it specifies the onset of adult development. Although a number of studies have addressed these functions for E93, little is known about its roles in the salivary gland where the E93 locus was originally identified. Here we show that E93 is required for development through late pupal stages, with mutants displaying defects in adult differentiation and no detectable effect on the destruction of salivary glands. RNA-seq analysis demonstrates that E93 regulates genes involved in development and morphogenesis in the salivary glands, but has little effect on cell death gene expression. We also show that E93 is required to direct the proper timing of ecdysone-regulated gene expression in salivary glands, and that it suppresses earlier transcriptional programs that occur during larval and prepupal stages. These studies support the model that the stage-specific induction of E93 in late prepupae provides a critical signal that defines the end of larval development and the onset of adult differentiation.

2022-08-11 | GSE181948 | GEO

Increased chromatin accessibility promotes the evolution of a transcriptional silencer in Drosophila [greenCUT&RUN]

Project description:The loss of discrete morphological traits, the most common evolutionary transition, is typically driven by changes in expression of developmental genes. Mutations accumulating in regulatory elements of these genes can disrupt DNA binding sites for transcription factors patterning their spatial expression, or delete entire enhancers. Regulatory elements, however, may in principle be silenced through other mechanisms, including changes in chromatin accessibility, or the emergence of repressive elements. Here, we show that an increase in chromatin accessibility at the pigmentation gene yellow, combined with the gain of a repressor site, underlie the evolutionary loss of a spot pigmentation pattern on the wings of a Drosophila species. The evolutionary gain of accessibility of this repressive element is regulated by E93, a transcription factor governing the progress of metamorphosis. This convoluted evolutionary scenario contrasts with the classical parsimonious mutational paths generally envisioned and often documented for morphological losses. It illustrates for the first time how evolutionary changes in chromatin accessibility may directly contribute to morphological diversification.

2023-02-17 | GSE222716 | GEO

Increased chromatin accessibility promotes the evolution of a transcriptional silencer in Drosophila [CUT&RUN]

2023-02-17 | GSE222715 | GEO

Increased chromatin accessibility promotes the evolution of a transcriptional silencer in Drosophila [ATAC-seq]

2023-02-17 | GSE222714 | GEO

Active DNA demethylation during the vertebrate phylotypic period

Project description:The vertebrate body plan and organs are shaped during a highly conserved embryonic phase called the phylotypic stage, however the mechanisms that guide the epigenome through this transition and their evolutionary conservation remain elusive. Here we report widespread DNA demethylation of thousands of enhancers during the phylotypic period in zebrafish, Xenopus and mouse. These dynamic enhancers are linked to essential developmental genes that display coordinated transcriptional and epigenomic changes in the diverse vertebrates during embryogenesis. Phylotypic stage-specific binding of Tet proteins to (hydroxy)methylated DNA, and enrichment of hydroxymethylcytosine on these enhancers, implicated active DNA demethylation in this process. Furthermore, loss of function of Tet1/2/3 in zebrafish caused reduced chromatin accessibility and increased methylation levels specifically on these enhancers, indicative of DNA methylation being an upstream regulator of phylotypic enhancer function. Overall, our study reveals a novel regulatory module associated with the most conserved phase of vertebrate embryogenesis and uncovers an ancient developmental role for the Tet dioxygenases.

2016-01-27 | PXD001164 | Pride

ATAC-seq in TX1072 XXΔXic and XO mESCs during differentiation

Project description:Developmental genes are controlled by complex cis-regulatory landscapes that integrate multiple signals to ensure the correct spatio-temporal expression pattern. To investigate the underlying regulatory principles, we use the Xist locus as a model, which encodes the master regulator of X-chromosome inactivation. Xist is upregulated at the primed pluripotent state in a female-specific manner, thus integrating developmental cues and X-dosage information. It remains poorly understood how these signals are decoded by the ~800kb genomic region that controls Xist. While a series of repressive cis-regulatory elements have been identified, the distal enhancers that activate Xist transcription remain largely unknown. Here we use ATAC-seq to profile DNA accessibility within the X inactivation center at the onset of random X-chromosome inactivation using an endogenous cell model of the inactive (TX 1072 XXΔXic) and active (TX 1072 XO) X chromosome.

2021-03-04 | GSE167350 | 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