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SPF45/RBM17-dependent, but not U2AF-dependent, splicing in a distinct subset of human short introns

Author

Listed:
  • Kazuhiro Fukumura

    (Division of Gene Expression Mechanism, Institute for Comprehensive Medical Science, Fujita Health University)

  • Rei Yoshimoto

    (Division of Gene Expression Mechanism, Institute for Comprehensive Medical Science, Fujita Health University
    Department of Applied Biological Sciences, Faculty of Agriculture, Setsunan University)

  • Luca Sperotto

    (Institute of Structural Biology, Helmholtz Zentrum München
    Bavarian NMR Center (BNMRZ), Chemistry Department, Technical University of Munich)

  • Hyun-Seo Kang

    (Institute of Structural Biology, Helmholtz Zentrum München
    Bavarian NMR Center (BNMRZ), Chemistry Department, Technical University of Munich)

  • Tetsuro Hirose

    (Graduate School of Frontier Biosciences, Osaka University)

  • Kunio Inoue

    (Graduate School of Science, Kobe University)

  • Michael Sattler

    (Institute of Structural Biology, Helmholtz Zentrum München
    Bavarian NMR Center (BNMRZ), Chemistry Department, Technical University of Munich)

  • Akila Mayeda

    (Division of Gene Expression Mechanism, Institute for Comprehensive Medical Science, Fujita Health University)

Abstract

Human pre-mRNA introns vary in size from under fifty to over a million nucleotides. We searched for essential factors involved in the splicing of human short introns by screening siRNAs against 154 human nuclear proteins. The splicing activity was assayed with a model HNRNPH1 pre-mRNA containing short 56-nucleotide intron. We identify a known alternative splicing regulator SPF45 (RBM17) as a constitutive splicing factor that is required to splice out this 56-nt intron. Whole-transcriptome sequencing of SPF45-deficient cells reveals that SPF45 is essential in the efficient splicing of many short introns. To initiate the spliceosome assembly on a short intron with the truncated poly-pyrimidine tract, the U2AF-homology motif (UHM) of SPF45 competes out that of U2AF65 (U2AF2) for binding to the UHM-ligand motif (ULM) of the U2 snRNP protein SF3b155 (SF3B1). We propose that splicing in a distinct subset of human short introns depends on SPF45 but not U2AF heterodimer.

Suggested Citation

  • Kazuhiro Fukumura & Rei Yoshimoto & Luca Sperotto & Hyun-Seo Kang & Tetsuro Hirose & Kunio Inoue & Michael Sattler & Akila Mayeda, 2021. "SPF45/RBM17-dependent, but not U2AF-dependent, splicing in a distinct subset of human short introns," Nature Communications, Nature, vol. 12(1), pages 1-12, December.
    • Handle: RePEc:nat:natcom:v:12:y:2021:i:1:d:10.1038_s41467-021-24879-y
    DOI: 10.1038/s41467-021-24879-y
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    Cited by:

    1. Lina Liu & Ana Vujovic & Nandan P. Deshpande & Shashank Sathe & Govardhan Anande & He Tian Tony Chen & Joshua Xu & Mark D. Minden & Gene W. Yeo & Ashwin Unnikrishnan & Kristin J. Hope & Yu Lu, 2022. "The splicing factor RBM17 drives leukemic stem cell maintenance by evading nonsense-mediated decay of pro-leukemic factors," Nature Communications, Nature, vol. 13(1), pages 1-17, December.

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