Drosophila melanogaster
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA239007 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1174370.fastq.gz | Fastqsanger.gz | |||
| SRR1174371.fastq.gz | Fastqsanger.gz | |||
| SRR1174372.fastq.gz | Fastqsanger.gz | |||
| SRR1174373.fastq.gz | Fastqsanger.gz | |||
| SRR1174374.fastq.gz | Fastqsanger.gz |
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Project description:In vivo crosslinking studies suggest that the Drosophila transcription factor Bicoid (Bcd) binds to several thousand sites during early embryogenesis, but it is not clear how many of these binding events are functionally important. In contrast, reporter gene studies have identified more than 60 Bcd-dependent enhancers, all of which contain clusters of the consensus binding sequence TAATCC. These studies also identified clusters of TAATCC motifs (inactive fragments) that failed to drive Bcd-dependent activation. In general, active fragments showed higher levels of Bcd-binding in vivo, and were enriched in predicted binding sites for the ubiquitous maternal protein Zelda (Zld). Here we test the role of Zld in Bcd-mediated binding and transcription. Removal of Zld function and mutations in Zld sites caused significant reductions in Bcd-binding to known enhancers, and variable effects on the activation and spatial positioning of Bcd-dependent expression patterns. Genome-wide binding experiments in Zld mutants showed variable effects on Bcd-binding peaks, ranging from strong reductions to significantly enhanced levels of binding. Increases in Bcd binding caused the precocious Bcd-dependent activation of genes that are normally not expressed in early embryos, suggesting that Zld controls the genome-wide binding profile of Bcd at the qualitative level, and is critical for selecting target genes for activation in the early embryo. These results underscore the importance of combinatorial binding in enhancer function, and provide data that will help predict regulatory activities based on DNA sequence. 1-3 hour wild type and zelda mutant embryos were examined for Bicoid binding using Illumina HiSeq 2000. The Bcd antibody is a rabbit polyclonal antiserum raised against full length Drosophila Bcd protein (Ochoa-Espinosa et al. 2009 PNAS). The antiserum was further purified using the Protein A Antibody Purification Kit (Sigma) for ChIP-seq.
2014-05-02 | E-GEOD-55256 | biostudies-arrayexpress
Project description:DamID profiling of neural transcription factor binding in Drosophila melanogaster embryos
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Project description:6mA-DNA-binding factor Jumu controls maternal-to-zygotic transition upstream of Zelda
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Project description:DamID profiling of proneural transcription factor binding in Drosophila melanogaster wing imaginal discs
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Project description:A conspicuous feature of early animal development is the lack of transcription from the embryonic genome, and it typically takes several hours to several days (depending on the species) until widespread transcription of the embryonic genome begins. Although this transition is ubiquitous, relatively little is known about how the shift from a transcriptionally quiescent to transcriptionally active genome is controlled. We describe here the genome-wide distributions and temporal dynamics of nucleosomes and post-translational histone modifications through the maternal-to-zygotic transition in embryos of the pomace fly Drosophila melanogaster. At mitotic cycle 8, when few zygotic genes are being transcribed, embryonic chromatin is in a relatively simple state: there are few nucleosome-free regions, undetectable levels of the histone methylation marks characteristic of mature chromatin, and low levels of histone acetylation at a relatively small number of loci. Histone acetylation increases by cycle 12, but it is not until cycle 14 that nucleosome-free regions and domains of histone methylation become widespread. Early histone acetylation is strongly associated with regions that we have previously shown are bound in early embryos by the maternally deposited transcription factor Zelda. Most of these Zelda-bound regions are destined to be enhancers or promoters active during mitotic cycle 14, and our data demonstrate that they are biochemically distinct long before they become active, raising the possibility that Zelda triggers a cascade of events, including the accumulation of specific histone modifications, that plays a role in the subsequent activation of these sequences. Many of these Zelda-associated active regions occur in larger domains that we find strongly enriched for histone marks characteristic of Polycomb-mediated repression, suggesting a dynamic balance between Zelda activation and Polycomb repression. Collectively, these data paint a complex picture of a genome in transition from a quiescent to an active state, and highlight the role of Zelda in mediating this transition. We performed genome-wide mapping of histone H3 and 9 types of histone modifications, including H4K5ac, H4K8ac, H3K4me1, H3K4me3, H3K27me3, H3K36me3, H3K9ac, H3K18ac, and H3K27ac by ChIP-seq, in hand-sorted wild-type Drosophila melanogaster embryos at 4 different development time points corresponding to mitotic cycle 7-9, 11-13, 14a-b, and 14c-d, respectively. We also carried out ChIP-seq experiments in zelda mutant embryos after showing that the deposition of histone marks in early embryos strongly correlated with the binding of Zelda in wild-type embryos.
2014-10-16 | E-GEOD-58935 | biostudies-arrayexpress
Project description:Zelda binding in the early Drosophila melanogaster embryo marks regions subsequently activated at the maternal-to-zygotic transition
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