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Splicing is the process by which eukaryotic RNA is edited before its translation into protein. The RNA strand transcribed from eukaryotic DNA is called the primary transcript. The primary transcripts that become mRNAs are called precursor messenger RNAs (pre-mRNAs). Eukaryotic pre-mRNA contains alternating sequences of exons and introns. Exons are nucleotide sequences that code for proteins, whereas introns are the non-coding regions. In RNA splicing, introns are removed and exons are bonded...
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Exon Junction Complex Shapes the Transcriptome by Repressing Recursive Splicing.

Lorea Blazquez1, Warren Emmett2, Rupert Faraway1

  • 1Department of Neuromuscular Diseases, UCL Queen Square Institute of Neurology, Queen Square, London WC1N 3BG, UK; The Francis Crick Institute, 1 Midland Road, London NW1 1AT, UK.

Molecular Cell
|November 3, 2018
PubMed
Summary
This summary is machine-generated.

The exon junction complex (EJC) represses recursive splicing (RS) of constitutive RS-exons and cryptic microexons. EJC factor deficiency causes RS-exon skipping, linked to microcephaly and human diseases.

Keywords:
RS exonalternative splicing mechanismsevolutionexon junction complexgene expressionmicrocephalymicroexonneurodevelopmental disordersrecursive splicing

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Area of Science:

  • Molecular Biology
  • Genetics
  • RNA Splicing

Background:

  • Recursive splicing (RS) involves specific exon-intron structures creating recursive splice sites.
  • Previous research primarily investigated cryptic RS-exons, overlooking annotated RS-exons.
  • The role of the exon junction complex (EJC) in regulating RS was not well understood.

Purpose of the Study:

  • To investigate the role of the EJC in repressing recursive splicing.
  • To identify factors involved in maintaining RS-exon inclusion.
  • To explore the evolutionary and disease relevance of RS regulation.

Main Methods:

  • Analysis of annotated and cryptic RS-exons across species.
  • Investigating the function of EJC core and peripheral factors (PNN, RNPS1) in spliceosomal assembly.
  • Studying the impact of EJC factor haploinsufficiency (Magoh) in a mouse model.

Main Results:

  • The EJC represses RS of hundreds of annotated RS-exons and blocks cryptic microexons by inhibiting spliceosome assembly.
  • Core EJC factors and PNN/RNPS1 maintain RS-exon inclusion.
  • Annotated RS-exons are prevalent in deuterostomes; cryptic RS-exons are more common in Drosophila.
  • Incomplete EJC repression contributes to physiological alternative splicing.
  • Magoh haploinsufficiency in mice leads to RS-exon skipping in the brain, relevant to microcephaly.

Conclusions:

  • The EJC is a key repressor of both constitutive and cryptic recursive splicing.
  • Dysregulation of RS by the EJC has implications for alternative splicing, evolution, and human diseases like microcephaly.