Although splicing is essential for the expression of most eukaryotic genes, 
inactivation of splicing factors causes specific defects in mitosis. The 
molecular cause of this defect is unknown. Here, we show that the spliceosome 
subunits SNW1 and PRPF8 are essential for sister chromatid cohesion in human 
cells. A transcriptome-wide analysis revealed that SNW1 or PRPF8 depletion 
affects the splicing of specific introns in a subset of pre-mRNAs, including 
pre-mRNAs encoding the cohesion protein sororin and the APC/C subunit APC2. SNW1 
depletion causes cohesion defects predominantly by reducing sororin levels, 
which causes destabilisation of cohesin on DNA. SNW1 depletion also reduces 
APC/C activity and contributes to cohesion defects indirectly by delaying 
mitosis and causing "cohesion fatigue". Simultaneous expression of sororin and 
APC2 from intron-less cDNAs restores cohesion in SNW1-depleted cells. These 
results indicate that the spliceosome is required for mitosis because it enables 
expression of genes essential for cohesion. Our transcriptome-wide 
identification of retained introns in SNW1- and PRPF8-depleted cells may help to 
understand the aetiology of diseases associated with splicing defects, such as 
retinosa pigmentosum and cancer.