An evolutionarily conserved, alternatively spliced, intron in the p68/DDX5 DEAD-box RNA helicase gene encodes a novel miRNA

Hayley C. Moore, Michael Johnston, Samantha M. Nicol, Jean-Christophe Bourdon, Alastair M. Thompson, Gyorgy Hutvagner (Lead / Corresponding author), Frances V. Fuller-Pace (Lead / Corresponding author)

    Research output: Contribution to journalArticlepeer-review

    14 Citations (Scopus)

    Abstract

    The DEAD-box RNA helicase p68 (DDX5) plays important roles in several cellular processes, including transcription, pre-mRNA processing, and microRNA (miRNA) processing. p68 expression is growth and developmentally regulated, and alterations in p68 expression and/or function have been implicated in tumor development. The p68 gene encodes an evolutionarily conserved, alternatively spliced, intron the function of which has to date remained unclear. Although the intron-containing p68 RNA does not appear to yield an alternative p68 protein, it is differentially expressed in cell lines and tissues, indicating regulation of expression. Here we show that the p68 conserved intron encodes a novel putative miRNA, suggesting a previously unknown possible regulatory function for the p68 intron. We show that this miRNA (referred to as p68 miRNA) is processed from the intron via the canonical miRNA-processing pathway and that it associates with the Argonaute protein Ago2. Finally we show that the p68 miRNA suppresses an mRNA bearing complementary target sequences, suggesting that it is functional. These findings suggest a novel mechanism by which alterations in p68 expression may impact on the cell.

    Original languageEnglish
    Pages (from-to)555-562
    Number of pages8
    JournalRNA: a Publication of the RNA Society
    Volume17
    Issue number4
    DOIs
    Publication statusPublished - Apr 2011

    Keywords

    • p68/DDX5
    • RNA helicase
    • alternatively spliced intron
    • miRNA
    • TRANSCRIPTIONAL COACTIVATOR
    • RIBOSOMAL-RNA
    • P68
    • EXPRESSION
    • PROTEIN
    • CANCER
    • IDENTIFICATION
    • DIFFERENTIATION
    • GROWTH
    • PROLIFERATION

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