Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Effect of mago nashi depletion on gene expression in Drosophila S2R+ cells


ABSTRACT: This study was designed to identify changes in gene expression resulting from depletion of Mago nashi (Mago), a core subunit of the exon junction complex. Drosophila S2R+ cells were treated with double-stranded RNA targeting either LacZ or Mago for 6 days. Poly(A)+ RNA was purified from each sample and sequenced using 54 bp reads on an Illumina Genome Analyzer II. Fold changes in expression were calculated for each gene as the ratio of the reads per kilobase per million reads (RPKM) for Mago relative to LacZ. In other experiments, we have shown that Mago is required for correct splicing of the MAP kinase gene and its depletion causes a large reduction in MAP kinase mRNA levels. MAP kinase is a large gene in heterochromatin. In this study, we find that heterochromatic genes are disproportionately down-regulated in Mago-depleted cells, and those with large introns are particularly likely to be affected. SRA accession number: SRP003001.1 Sequencing of poly(A)+ RNA from S2R+ cells treated with either lacZ (control) or mago (experimental) dsRNA

ORGANISM(S): Drosophila melanogaster

SUBMITTER: Jessica Treisman 

PROVIDER: E-GEOD-23997 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Exon junction complex subunits are required to splice Drosophila MAP kinase, a large heterochromatic gene.

Roignant Jean-Yves JY   Treisman Jessica E JE  

Cell 20101001 2


The exon junction complex (EJC) is assembled on spliced mRNAs upstream of exon-exon junctions and can regulate their subsequent translation, localization, or degradation. We isolated mutations in Drosophila mago nashi (mago), which encodes a core EJC subunit, based on their unexpectedly specific effects on photoreceptor differentiation. Loss of Mago prevents epidermal growth factor receptor signaling, due to a large reduction in MAPK mRNA levels. MAPK expression also requires the EJC subunits Y1  ...[more]

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