Back

Inhibition of PfCLK3 a master regulator of malaria parasite RNA-splicing provides the basis for a radical cure for malaria

Janha, O.; Olaniyan, N.; Diam, G. K.; Sharma, S.; Beraldi, D.; Jamieson, A.; Bozdech, Z.; Tobin, A. B.; Modrzynska, K.

2025-10-07 molecular biology
10.1101/2025.10.07.680601 bioRxiv
Show abstract

Emerging resistance to front-line anti-malarials means there is a race to discover new drugs with novel mechanisms of action that remain effective across multiple stages of the parasite life cycle. Previously we reported the malaria protein kinase, PfCLK3, as a target offering a cure, prophylaxis and transmission blocking. The homology between PfCLK3 and human kinases suggested that the mechanism of parasiticidal activity of PfCLK3 inhibitors is disruption of RNA processing. Here, we use whole genome RNA-sequencing to reveal that selective PfCLK3 inhibition extensively affects RNA-splicing with 2039 splice-junctions across 1125 genes mis-spliced in treated wild type parasites compared to controls. The function of mis-spliced transcripts showed that the affected genes were involved in numerous essential parasite processes associated with multiple life cycle stages and revealed transcripts and introns particularly susceptible to inhibition. Our study supports the role of PfCLK3 as an important regulator of spliceosome activity and establishes the distinct mechanism of parasiticidal activity of PfCLK3 inhibitors from current front-line treatments.

Matching journals

The top 6 journals account for 50% of the predicted probability mass.

50% of probability mass above

"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.