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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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JIL kinase - marker of active chromatin and sensor of dosage compensation

ABSTRACT: ChIP-chip profiles of RNA Polymerase II phosphorylated on serine 2 in Drosophila S2 cells. RNA Polymerase II phosphorylated on serine 2 ChIP in Drosophila S2 cells. 3 biological replicates with dye-swaps.

ORGANISM(S): Drosophila melanogaster

SUBMITTER: Tobias Straub

PROVIDER: E-GEOD-37784 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Chromosomal kinase JIL-1 in Drosophila S2 Cells

Project description:This SuperSeries is composed of the following subset Series: GSE22618: JIL kinase – marker of active chromatin and sensor of dosage compensation GSE22620: JIL-1 RNAi in Drosophila S2 Cells Refer to individual Series

2011-02-01 | E-GEOD-22621 | biostudies-arrayexpress

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Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

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Project description:We identified 131 high affinity sites of the Drosophila DCC combining residual ChIP-chip profiles after differential crosslinking and RNAi-mediated knockdown of spreading factors Keywords: ChIP-chip MSL1 and MSL2 ChIP under various conditions including differential crosslinking and RNAi against MOF, MLE and MSL3. 2-4 replicates per experiment. dye-swaps as indicated in sample description.

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Project description:The H4K16 acetyltransferase MOF plays a crucial role in dosage compensation in Drosophila, but has additional, global functions. We compared the molecular context and effect of MOF in male and female flies combining chromosome-wide mapping and transcriptome studies with analyses of defined reporter loci in transgenic flies. MOF distributes dynamically between two complexes, the Dosage Compensation Complex and a complex containing MBD-R2, a global facilitator of transcription. These different targeting principles define the distribution of MOF between the X chromosome and autosomes and at transcription units with 5’ or 3’ enrichment. The male X chromosome differs from all other chromosomes in that H4K16 acetylation levels do not correlate with transcription output. The reconstitution of this phenomenon at a model locus revealed that the activation potential of MOF is constraint in male cells in the context of the DCC to arrive at the two-fold activation of transcription characteristic of dosage compensation. ChIP-chip profiling of MBD-R2, MOF and MSL1 in adult male and female flies, and SL2 cells, incl. at least 3 biological replicates

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