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

Kazuhiro Fukumura (), Rei Yoshimoto, Luca Sperotto, Hyun-Seo Kang, Tetsuro Hirose, Kunio Inoue, Michael Sattler and Akila Mayeda ()
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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
Luca Sperotto: Institute of Structural Biology, Helmholtz Zentrum München
Hyun-Seo Kang: Institute of Structural Biology, Helmholtz Zentrum München
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
Akila Mayeda: Division of Gene Expression Mechanism, Institute for Comprehensive Medical Science, Fujita Health University

Nature Communications, 2021, vol. 12, issue 1, 1-12

Abstract: 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.

Date: 2021
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DOI: 10.1038/s41467-021-24879-y

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