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Survival motor neuron (SMN) functions in the assembly of spliceosomal small nuclear ribonucleoproteins (snRNPs) that catalyze pre-mRNA splicing. Here, we used disruptions in  Smn  and two additional snRNP biogenesis genes,  Phax  and  Ars2 , to classify RNA processing differences as snRNP-dependent or gene-specific in  Drosophila .  Phax  and  Smn  mutants exhibited comparable reductions in snRNAs, and comparison of their transcriptomes uncovered shared sets of RNA processing changes. In contrast,  Ars2  mutants displayed only small decreases in snRNA levels, and RNA processing changes in these mutants were generally distinct from those identified in  Phax  and  Smn  animals. Instead, RNA processing changes in  Ars2  mutants support the known interaction of Ars2 protein with the cap-binding complex, as splicing changes showed a clear bias toward the first intron. Bypassing disruptions in snRNP biogenesis, direct knockdown of spliceosomal proteins caused similar changes in the splicing of snRNP-dependent events. However, these snRNP-dependent events were largely unaltered in three  Smn  mutants expressing missense mutations that were originally identified in human spinal muscular atrophy (SMA) patients. Hence, findings here clarify the contributions of Phax, Smn, and Ars2 to snRNP biogenesis in  Drosophila , and loss-of-function mutants for these proteins reveal differences that help disentangle cause and effect in SMA model flies.

Transcriptomic comparison of <i>Drosophila</i> snRNP biogenesis mutants reveals mutant-specific changes in pre-mRNA processing: implications for spinal muscular atrophy

Transcriptomic comparison of Drosophila snRNP biogenesis mutants reveals mutant-specific changes in pre-mRNA processing: implications for spinal muscular atrophy