1. SAP30BP interacts with RBM17/SPF45 to promote splicing in a subset of human short introns.
- Author
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Fukumura K, Sperotto L, Seuß S, Kang HS, Yoshimoto R, Sattler M, and Mayeda A
- Subjects
- Humans, Introns genetics, Splicing Factor U2AF genetics, Splicing Factor U2AF metabolism, RNA Splicing Factors genetics, RNA Splicing Factors metabolism, Ribonucleoprotein, U2 Small Nuclear genetics, Transcription Factors metabolism, RNA Precursors metabolism, Nuclear Proteins genetics, Nuclear Proteins metabolism, RNA Splicing genetics, Spliceosomes metabolism
- Abstract
Human pre-mRNA splicing requires the removal of introns with highly variable lengths, from tens to over a million nucleotides. Therefore, mechanisms of intron recognition and splicing are likely not universal. Recently, we reported that splicing in a subset of human short introns with truncated polypyrimidine tracts depends on RBM17 (SPF45), instead of the canonical splicing factor U2 auxiliary factor (U2AF) heterodimer. Here, we demonstrate that SAP30BP, a factor previously implicated in transcriptional control, is an essential splicing cofactor for RBM17. In vitro binding and nuclear magnetic resonance analyses demonstrate that a U2AF-homology motif (UHM) in RBM17 binds directly to a newly identified UHM-ligand motif in SAP30BP. We show that this RBM17-SAP30BP interaction is required to specifically recruit RBM17 to phosphorylated SF3B1 (SF3b155), a U2 small nuclear ribonucleoprotein (U2 snRNP) component in active spliceosomes. We propose a mechanism for splicing in a subset of short introns, in which SAP30BP guides RBM17 in the assembly of active spliceosomes., Competing Interests: Declaration of interests The authors declare no competing interests., (Copyright © 2023 The Author(s). Published by Elsevier Inc. All rights reserved.)
- Published
- 2023
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