N6-methyladenosine (m6A) is the most abundant internal modification of eukaryotic mRNA. This modification has previously been shown to alter the export kinetics for mRNAs though the molecular details surrounding this phenomenon remain poorly understood. Here we show that the m6A complex (WTAP, KIAA1429, METTL3/14) drives recruitment of the TREX mRNA export complex onto m6A modified mRNAs and this process is essential for the efficient export of certain mRNAs. Depletion of the core m6A complex leads to loss of TREX from mRNAs which undergo the m6A modification. We show that TREX stimulates recruitment of the m6A reader protein YTHDC1 to the mRNP and the m6A complex influences the interaction of TREX with YTHDC1. We suggest that m6A acts as a surrogate for other TREX recruitment mechanisms such as splicing and 5' capping, in long internal and final exons which may otherwise be devoid of this essential complex for mRNA export. Overall design: mRNA profiles of control and Virilizer/WTAP RNAi samples in cytoplasmic and nuclear cell fractions generated by mRNA-seq in triplicate using HiSeq 2500
The m<sup>6</sup>A-methylase complex recruits TREX and regulates mRNA export.
Cell line, Subject
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Identification of candidate genes involved in neuroblastoma progression by combining genomic and expression microarrays with survival data.
Sex, Age
View SamplesGene expression analysis was performed on 30 Neuroblastomas to identify genes whose transcription is significantly altered by recurrent chromosomal alterations. Genomic copy number losses and gains had been delineated in the tumours using FISH and SNP arrays. We have identified genes significantly altered by 7 recurrent alterations: 1p, 3p, 4p, 10q and 11q loss, 2p and 17q gain, and genes co-amplified and over-expressed as a result of MYCN amplification.
Identification of candidate genes involved in neuroblastoma progression by combining genomic and expression microarrays with survival data.
Sex, Age
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