Skipping of an alternative intron in the srsf1 3' untranslated region increases transcript stability

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Author(s)

    • Akaike Yoko
    • Department of Stress Science, Institute of Health Biosciences, the University of Tokushima Graduate School|Student Lab, the University of Tokushima Faculty of Medicine
    • Kurokawa Ken
    • Department of Stress Science, Institute of Health Biosciences, the University of Tokushima Graduate School|Student Lab, the University of Tokushima Faculty of Medicine
    • Kajita Keisuke
    • Department of Stress Science, Institute of Health Biosciences, the University of Tokushima Graduate School|Student Lab, the University of Tokushima Faculty of Medicine
    • Kuwano Yuki
    • Department of Stress Science, Institute of Health Biosciences, the University of Tokushima Graduate School
    • Masuda Kiyoshi
    • Department of Stress Science, Institute of Health Biosciences, the University of Tokushima Graduate School
    • Nishida Kensei
    • Department of Stress Science, Institute of Health Biosciences, the University of Tokushima Graduate School
    • Wan Kang Seung
    • Institute of Complementary and Integrative Medicine, Medical Research Center, Seoul National University
    • Tanahashi Toshihito
    • Department of Stress Science, Institute of Health Biosciences, the University of Tokushima Graduate School
    • Rokutan Kazuhito
    • Department of Stress Science, Institute of Health Biosciences, the University of Tokushima Graduate School

Abstract

The <I>srsf1</I> gene encodes serine/arginine-rich splicing factor 1 (SRSF1) that participates in both constitutive and alternative splicing reactions. This gene possesses two ultraconserved elements in the 3’ untranslated region (UTR). Skipping of an alternative intron between the two elements has no effect on the protein-coding sequence, but it generates a premature stop codon (PTC)-containing mRNA isoform, whose degradation is considered to depend on nonsense-mediated mRNA decay (NMD). However, several cell lines (HCT116, RKO, HeLa, and WI38 cells) constitutively expressed significant amounts of the <I>srsf1</I> PTC variant. HCT116 cells expressed the PTC variant nearly equivalent to the major isoform that includes the alternative intron in the 3’ UTR. Inhibition of NMD by silencing a key effecter UPF1 or by treatment with cycloheximide failed to increase amounts of the PTC variant in HCT116 cells, and the PTC variant was rather more stable than the major isoform in the presence of actinomycin D. Our results suggest that the original stop codon may escape from the NMD surveillance even in skipping of the alternative intron. The <I>srsf1</I> gene may produce an alternative splice variant having truncated 3’ UTR to relief the microRNA- and/or RNA-binding protein-mediated control of translation or degradation. J. Med. Invest. 58: 180-187, August, 2011

Journal

  • The Journal of Medical Investigation

    The Journal of Medical Investigation 58(3,4), 180-187, 2011

    The University of Tokushima Faculty of Medicine

Codes

  • NII Article ID (NAID)
    130004822655
  • NII NACSIS-CAT ID (NCID)
    AA11166929
  • Text Lang
    ENG
  • Article Type
    journal article
  • ISSN
    1343-1420
  • Data Source
    IR  J-STAGE 
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