Leela N.Prommana P.Kamchonwongpaisan S.Taechalertpaisarn T.Shaw P.J.Mahidol University2024-02-192024-02-192024-01-01PeerJ Vol.12 (2024)https://repository.li.mahidol.ac.th/handle/123456789/97240Background. Plasmodium falciparum possesses a cobalamin-dependent methionine synthase (MS). MS is putatively encoded by the PF3D7_1233700 gene, which is orthologous and syntenic in Plasmodium. However, its vulnerability as an antimalarial target has not been assessed. Methods. We edited the PF3D7_1233700 and PF3D7_0417200 (dihydrofolate reductase-thymidylate synthase, DHFR-TS) genes and obtained transgenic P. falciparum parasites expressing epitope-tagged target proteins under the control of the glmS ribozyme. Conditional loss-of-function mutants were obtained by treating transgenic parasites with glucosamine. Results. DHFR-TS, but not MS mutants showed a significant proliferation defect over 96 h, suggesting that P. falciparum MS is not a vulnerable antimalarial target.NeuroscienceBiochemistry, Genetics and Molecular BiologyAgricultural and Biological SciencesArticleSCOPUS10.7717/peerj.165952-s2.0-8518474782521678359