3 results for chip-seq drosophila
Data from: A global change in RNA polymerase II pausing during the Drosophila midblastula transition
Contributors: Chen, Kai, Johnston, Jeff, Shao, Wanqing, Meier, Samuel, Staber, Cynthia, Zeitlinger, Julia
ChIP-seq experiments on tightly staged Drosophila embryos and show that...ChIP-seq enrichment values at the transcription start site (TSS) and transcription...Drosophila melanogaster...Drosophila embryos and show that massive recruitment of RNA polymerase...Drosophila midblastula transition ... Massive zygotic transcription begins in many organisms during the midblastula transition when the cell cycle of the dividing egg slows down. A few genes are transcribed before this stage but how this differential activation is accomplished is still an open question. We have performed ChIP-seq experiments on tightly staged Drosophila embryos and show that massive recruitment of RNA polymerase II (Pol II) with widespread pausing occurs de novo during the midblastula transition. However, ∼100 genes are strongly occupied by Pol II before this timepoint and most of them do not show Pol II pausing, consistent with a requirement for rapid transcription during the fast nuclear cycles. This global change in Pol II pausing correlates with distinct core promoter elements and associates a TATA-enriched promoter with the rapid early transcription. This suggests that promoters are differentially used during the zygotic genome activation, presumably because they have distinct dynamic properties.
Data from: The Drosophila HNF4 nuclear receptor promotes glucose-stimulated insulin secretion and mitochondrial function in adults
Contributors: Thummel, Carl S., Barry, William E.
Drosophila melanogaster dm3 genome assembly. Transcripts meeting a cutoff...Drosophila melanogaster...ChIP-seq (MACS2) run with a peak shift of 100 bp. Enrichment peaks were...Drosophila HNF4 recapitulates hallmark symptoms of MODY1, including adult-onset...Drosophila HNF4 nuclear receptor promotes glucose-stimulated insulin secretion ... Although mutations in HNF4A were identified as the cause of Maturity Onset Diabetes of the Young 1 (MODY1) two decades ago, the mechanisms by which this nuclear receptor regulates glucose homeostasis remain unclear. Here we report that loss of Drosophila HNF4 recapitulates hallmark symptoms of MODY1, including adult-onset hyperglycemia, glucose intolerance and impaired glucose-stimulated insulin secretion (GSIS). These defects are linked to a role for dHNF4 in promoting mitochondrial function as well as the expression of Hex-C, a homolog of the MODY2 gene Glucokinase. dHNF4 is required in the fat body and insulin-producing cells to maintain glucose homeostasis by supporting a developmental switch toward oxidative phosphorylation and GSIS at the transition to adulthood. These findings establish an animal model for MODY1 and define a developmental reprogramming of metabolism to support the energetic needs of the mature animal.
Contributors: Kok, Kurtulus, Ay, Ahmet, Li, Li M., Arnosti, David N.
Drosophila melanogaster...ChIP-Seq experiments were visualized as custom tracks using Integrative...Drosophila embryos. This long-range repressor mediates histone acetylation...Drosophila Genome Oligo Microarrays (Agilent). Slide image data was quantified ... Metazoan transcriptional repressors regulate chromatin through diverse histone modifications. Contributions of individual factors to the chromatin landscape in development is difficult to establish, as global surveys reflect multiple changes in regulators. Therefore, we studied the conserved Hairy/Enhancer of Split family repressor Hairy, analyzing histone marks and gene expression in Drosophila embryos. This long-range repressor mediates histone acetylation and methylation in large blocks, with highly context-specific effects on target genes. Most strikingly, Hairy exhibits biochemical activity on many loci that are uncoupled to changes in gene expression. Rather than representing inert binding sites, as suggested for many eukaryotic factors, many regions are targeted errantly by Hairy to modify the chromatin landscape. Our findings emphasize that identification of active cis-regulatory elements must extend beyond the survey of prototypical chromatin marks. We speculate that this errant activity may provide a path for creation of new regulatory elements, facilitating the evolution of novel transcriptional circuits.