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Background  RBM10 is an RNA binding protein involved in message stabilization and alternative splicing regulation. The objective of the research described herein was to identify novel targets of RBM10-regulated splicing. To accomplish this, we downregulated RBM10 in human cell lines, using small interfering RNAs, then monitored alternative splicing, using a reverse transcription-PCR screening platform.    Results  RBM10 knockdown (KD) provoked alterations in splicing events in 10–20% of the pre-mRNAs, most of which had not been previously identified as RBM10 targets. Hierarchical clustering of the genes affected by RBM10 KD revealed good conservation of alternative exon inclusion or exclusion across cell lines. Pathway annotation showed  RAS  signaling to be most affected by RBM10 KD. Of particular interest was the finding that splicing of  SMN  pre-mRNA, encoding the survival of motor neuron (SMN) protein, was influenced by RBM10 KD. Inhibition of RBM10 resulted in preferential expression of the full-length, exon 7 retaining,  SMN  transcript in four cancer cell lines and one normal skin fibroblast cell line. SMN protein is expressed from two genes,  SMN1  and  SMN2 , but the  SMN1  gene is homozygously disrupted in people with spinal muscular atrophy; as a consequence, all of the SMN that is expressed in people with this disease is from the  SMN2  gene. Expression analyses using primary fibroblasts from control, carrier and spinal muscle atrophy donors demonstrated that RBM10 KD resulted in preferential expression of the full-length, exon 7 retaining,  SMN2  transcript. At the protein level, upregulation of the full-length SMN2 was also observed. Re-expression of RBM10, in a stable RBM10 KD cancer cell line, correlated with a reversion of the KD effect, demonstrating specificity.    Conclusion  Our work has not only expanded the number of pre-mRNA targets for RBM10, but identified RBM10 as a novel regulator of  SMN2  alternative inclusion.    Electronic supplementary material  The online version of this article (doi:10.1186/s12867-017-0096-x) contains supplementary material, which is available to authorized users.

Splicing arrays reveal novel RBM10 targets, including SMN2 pre-mRNA