Malaria parasites can only reproduce sexually when they are in the gut of the mosquito, after it has ingested the precursor parasite cells present in an infected person's blood— a vulnerable stage of the parasite's complicated life cycle.
When malaria parasites are cultured in the lab for a long time through multiple cycles, they can lose the ability to reproduce and stop producing precursor cells to the sexual male and female form. The research team generated three cell lines of malaria parasite which could no longer reproduce in the lab and sequenced them. They found that there was a common mutation to the ap2-g gene across all three cell lines, a strong indication that the gene was involved in sexual reproduction. To confirm these observations, the team silenced the ap2-g gene in parasites that were still reproducing in the lab and found that they lost the ability to generate sexual stage parasites.
The full paper has been published in Nature:
Sinha et al. A cascade of DNA binding proteins for sexual commitment and development in Plasmodium. Nature. 2014 Mar 13;507(7491):253-7. doi: 10.1038/nature12970. Epub 2014 Feb 23.
Alongside a second paper separately detailing the role of AP2-G as a master switch:
Kafsack et al. A transcriptional switch underlies commitment to sexual development in human malaria parasites, Nature. 2014 Mar 13;507(7491):248-52. doi: 10.1038/nature12920. Epub 2014 Feb 23.