Discovery of a subset of human short introns that are spliced out by a novel mechanism

The well-known essential pre-mRNA splicing factor U2AF heterodimer (U2AF2–U2AF1) has been identified as mediating early splicing reactions in all introns of different lengths. However, Dr. Kazuhiro Fukumura in the Akila Mayeda lab at Fujita Health University has discovered that a subset of short introns with truncated polypyrimidine tracts are spliced by the RBM17–SAP30BP complex instead of U2AF heterodimer. Dr. Fukumura's team has proposed a unique mechanism in which SAP30BP guides RBM17 to active early spliceosomes.