The malaria parasite, Plasmodium falciparum, undergoes significant morphological changes throughout its lifecycle stages. Accordingly, transcription of genes in P. falciparum is tightly regulated in a stage-dependent manner. These transcriptional changes have been described by numerous RNA-seq studies and several key transcription factors have now been identified. However, post-transcriptional control of gene expression is less-well characterised in the malaria parasite. Alternative splicing of mRNA can produce transcripts that vary in their coding output as well as their nuclear export and stability. In mammals, alternative splicing is important for differentiation of cells and tissues. We are investigating the contribution of alternative splicing to the differentiation of parasites during their lifecycle. To achieve this, we are studying putative mediators of alternative splicing in P. falciparum: SR proteins and SR protein kinases. The SR proteins are Serine-Arginine repeat RNA-binding proteins that can regulate the interaction of the spliceosome with mRNA. SR protein kinases regulate the localisation and activity of SRs. We have used a CRISPR approach to create epitope-tagged, inducible knockdown/knockout parasite lines for six different SR proteins and three SR protein kinases. We have determined the subcellular localisation of each of these proteins and find varying degrees of nuclear and nucleo/cytoplasmic localisation. We have successfully induced disruption of SR and SR protein kinase gene expression in these lines, and have tested impacts on parasite growth, as well as RNA-seq analysis of splicing effects.