Drosophila melanogaster
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA273997 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1779550.fastq.gz | Fastqsanger.gz | |||
| SRR1779560.fastq.gz | Fastqsanger.gz | |||
| SRR1779570.fastq.gz | Fastqsanger.gz | |||
| SRR1779551.fastq.gz | Fastqsanger.gz | |||
| SRR1779561.fastq.gz | Fastqsanger.gz |
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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:The earliest stages of development in most metazoans are driven by maternally deposited proteins and mRNAs, with widespread transcriptional activation of the zygotic genome occurring hours after fertilization, at a period known as the maternal-to-zygotic transition (MZT). In Drosophila, the MZT is preceded by the transcription of a small number of genes that initiate sex determination, patterning and other essential developmental processes. The zinc-finger transcription factor Zelda (ZLD) plays a key role in the transcriptional activation of these earliest-expressed genes. To better understand the mechanisms of ZLD activation and the range of its targets, we used chromatin immunoprecipitation coupled with high-throughput sequencing (ChIP-Seq) to map regions bound by ZLD prior to (mitotic cycles 8 and 9), during (mitotic cycles 13 and early 14) and after (late mitotic cycle 14) the MZT. Although only a handful of genes are transcribed prior to mitotic cycle 10, we identified thousands of regions bound by ZLD in cycle 8-9 embryos, most of which remain bound through mitotic cycle 14. As expected, these ZLD-bound regions include the promoters and enhancers of the small subset of genes transcribed at this early stage. However we also observed ZLD bound at cycle 8-9 to the promoters of a large fraction of the several thousand genes whose first transcription does not occur until roughly an hour and four mitotic cycles later. These early ZLD-bound regions include virtually all of the thousands of known and presumed enhancers bound at cycle 14 by the transcription factors that regulate patterned gene activation during the MZT. The association between early ZLD binding and MZT activity is so strong that ZLD binding alone can be used to identify active promoters and regulatory sequences with high specificity and selectivity. This strong early association of ZLD with regions not active until the MZT suggests that ZLD is not only required for the earliest wave of transcription, but also plays a major role in activating the genome at the MZT. Genome-wide mapping of Zelda in wild-type Drosophila melanogaster embryos prior (mitotic cycles 8-9), during (cycles 13-14), and after (late cycle 14) maternal-to-zygotic transition
2011-07-18 | E-GEOD-30757 | biostudies-arrayexpress
Project description:During the first stages of development, the fertilized germ cells rapidly transition to totipotency. Maternally deposited mRNAs encode the proteins necessary for reprogramming the transcriptionally quiescent zygotic genome during this maternal-to-zygotic transition (MZT). The transcription factor Zelda is essential for this reprogramming in the Drosophila embryo. Zelda is necessary for transcriptional activation of the zygotic genome, and the absence of Zelda leads to embryonic lethality during the MZT. Excess Zelda activity is also lethal to the embryo, demonstrating that Zelda levels must be precisely controlled during early development. Because Zelda is encoded by a maternally deposited mRNA, Zelda levels in the embryo are controlled at the level of translation. To understand how levels of this essential reprogramming factor were regulated to allow for embryonic development and zygotic genome activation, we investigated the factors that regulated translation of zelda. Brain Tumor (BRAT) is a translational regulator that was previously shown to bind to zelda mRNA in the embryo. We showed that BRAT functions to repress zelda translation, as embryos deficient for maternal BRAT activity prematurely express Zelda. We further showed that in the larval brain, BRAT similarly regulates Zelda levels and identified specific BRAT-binding sites that mediate these effects. Thus, BRAT regulates Zelda in multiple tissues. Because both too little and too much Zelda are lethal to the embryo, we hypothesized that precocious expression of this transcriptional activator might be capable of driving precocious activation of the zygotic genome, leading to embryonic lethality. To test this hypothesis, we performed single embryo RNA-seq at distinct nuclear cycles throughout zygotic genome activation (NC10, NC12, NC13, and NC14) in control and brat-mutant embryos. Our results conclusively demonstrated that in embryos lacking functional BRAT, Zelda target genes were not prematurely activated. Rather, these genes were expressed normally, but become significantly upregulated at nuclear cycle 14, when the division cycle slows. Our data support a model in which zygotic genome activation requires precise coordination between expression of reprogramming factors, such as Zelda, and the slowing of the cell cycle.
2022-06-17 | GSE197582 | GEO
Project description:Zelda determines chromatin accessibility during the Drosophila maternal-to-zygotic transition
| PRJNA275186 | ENA
Project description:Immediately after fertilization the genome is transcriptionally quiescent. Maternally encoded pioneer transcription factors reprogram the chromatin state and facilitate the transcription of the zygotic genome. In Drosophila, transcription is initiated by the pioneer factor Zelda. While Zelda-occupied sites are enriched with histone acetylation, a post-translational mark associated with active cis-regulatory regions, the functional relationship between Zelda and histone acetylation in zygotic genome activation remained unclear. We show that Zelda-mediated recruitment of the histone acetyltransferase CBP is essential for zygotic transcription and embryonic development. CBP catalytic activity is necessary for release of RNA Polymerase II (Pol II) into transcription elongation. However, CBP largely activates zygotic transcription independent of acetylation through Pol II recruitment. Neither acetylation nor CBP are required for the pioneering function of Zelda. Our data suggest that pioneer factor-mediated recruitment of CBP is a conserved mechanism required to activate zygotic transcription but that this role is separable from the function of pioneer factors in restructuring chromatin accessibility.
2024-10-15 | GSE274629 | GEO
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.
2014-10-16 | GSE58935 | GEO
Project description:A central question in biology is how enhancers are made accessible. The Drosophila embryo is a good model system to study this question as the gene regulatory networks regulating early developmental events have been well characterized. Zelda (Zld) is a uniformly distributed transcription factor (TF) integral to these networks, acting prior to and in collaboration with the patterning TFs to regulate target enhancers. Here we test the hypothesis that Zld directs TF binding, examplified by Dorsal (Dl) which patterns the dorsoventral axis, across the genome by displacing nucleosomes at enhancers. By performing ChIP-seq and MNase-seq experiments on early embryos with or without Zld, we demonstrated that early enhancers are characterized by an intrinsically high nucleosome barrier, which is overcome by Zld, and that without Zld, Dl binding decreases at enhancers and redistributes to open regions devoid of enhancer activity. We propose that enhancers are initially specified across the genome by the binding of Zld, which locally decreases nucleosome occupancy, thereby assisting TFs in accessing their binding motifs and promoting transcriptional activity. Zld, Dl, Pol II ChIP-seq and MNase-seq profiles comparing 2-3h wild-type (wt) and zld- embryos, and MNase-seq profiles comparing 2-4h wt and gd7 embryos, all in 2 replicates
2015-08-21 | E-GEOD-65441 | biostudies-arrayexpress
Project description:In nearly all metazoans, the earliest stages of development are controlled by maternally deposited mRNAs and proteins. The zygotic genome only becomes transcriptionally active hours later. Transcriptional activation is tightly coordinated with the degradation of maternally provided mRNAs during this maternal-to-zygotic transition (MZT). In Drosophila melanogaster, the transcription factor Zelda plays an essential role in widespread activation of the zygotic genome. While Zelda expression is required both maternally and zygotically, the mechanisms by which it functions both during and after the MZT remain unclear. Zelda is a large protein with six C2H2 zinc fingers, but no additional identified domains or predicted enzymatic activities. Using Cas9-mediated genome editing to generate targeted mutations in Zelda, we determined the functional relevance of protein domains conserved amongst Zelda orthologs. Generating these mutations in vivo revealed that neither a conserved N-terminal zinc finger nor an acidic patch were required for activity. Similarly, using a variety of Cas9-enabled approaches we showed that a previously identified splice isoform of zelda is dispensable for viability, and the predicted protein product is not expressed at detectable levels. By contrast, we identified a highly conserved zinc-finger domain that is essential for the maternal, but not zygotic functions of Zelda. A mutation in this zinc-finger domain does not interfere with the capacity of Zelda to activate transcription, but rather leads to a hyperactive form of the protein and enhanced Zelda-dependent gene expression. Embryos inheriting this allele from their mothers die late in embryogenesis. These data define a protein domain critical for controlling Zelda activity and, for the first time, identify a separation between the maternal and zygotic requirements for Zelda. This demonstrates that highly regulated levels of Zelda activity are essential for establishing the developmental program during the MZT and that failure to precisely execute this program leads to embryonic lethality.
2017-11-28 | GSE103914 | GEO
Project description:Reprogramming cell fate during the first stages of embryogenesis requires that transcriptional activators gain access to the genome and remodel the zygotic transcriptome. Nonetheless, it is not clear if the continued activity of these pioneering factors is required throughout zygotic genome activation or if they are only required early to establish cis-regulatory regions. To address this question, we developed an optogenetic strategy to rapidly and reversibly inactivate the master regulator of genome activation in Drosophila, Zelda. Using this strategy, we demonstrated that continued Zelda activity is required throughout genome activation. We showed that Zelda binds DNA in the context of nucleosomes and suggest that this allows Zelda to occupy the genome despite the rapid division cycles in the early embryo. These data identify a powerful strategy to inactivate transcription factor function during development and suggest that reprogramming in the embryo may require specific, continuous pioneering functions to activate the genome.
2019-02-06 | GSE121157 | GEO
Project description:A long-standing question in the field of embryogenesis is how the zygotic genome is precisely activated by maternal factors, allowing normal early embryonic development. We have previously shown that N6-methyladenine (6mA) DNA modification is highly dynamic in early Drosophila embryos and forms an epigenetic mark. However, little is known about how 6mA-formed epigenetic information is decoded. Here we report that the Fox-family protein Jumu binds 6mA-marked DNA and acts as a maternal factor to regulate the maternal-to-zygotic transition. We find that zelda encoding the pioneer factor Zelda is marked by 6mA. Our genetic assays suggest that Jumu controls the proper zygotic genome activation (ZGA) in early embryos, at least in part, by regulating zelda expression. Thus, our findings not only support that the 6mA-formed epigenetic can be read by specific transcription factors, but also uncover a mechanism by which the Jumu regulates ZGA partially through Zelda in early embryos.
2019-04-18 | GSE86795 | GEO