Transcription Factor 25 Modulates Gametocytogenesis in the Malaria Parasite Plasmodium falciparum [RNA-Seq]

This study elucidates the role of TCF25 as a transcriptional regulator orchestrating sexual conversion in Plasmodium falciparum. Through generation of isogenic tcf25_ko parasite lines, we performed comparative transcriptomic analysis of synchronized ring-stage and schizont-stage parasites (WT vs knockout). Our data demonstrate that tcf25 deletion causes significant dysregulation of both gametocytogenesis-associated genes and antigenic variation gene families. TCF25 directly binds a sexual conversion regulator ap2-g4. These results indicate TCF25 as an essential upstream regulator of malaria parasite sexual development and potential transmission-blocking target. RNA-seq profiling was performed on Plasmodium falciparum at distinct intraerythrocytic stages (ring and schizont).

本研究阐明了转录调控因子TCF25在恶性疟原虫（Plasmodium falciparum）性转化过程中的核心调控作用。本研究通过构建同基因背景的tcf25敲除（tcf25_ko）寄生虫株，对同步化的环状体期与裂殖体期疟原虫（野生型与敲除型）开展了比较转录组分析。数据表明，敲除tcf25会导致配子体发生相关基因与抗原变异基因家族均出现显著表达紊乱。TCF25可直接结合性转化调控因子AP2-G4。上述结果证实，TCF25是疟原虫有性发育的关键上游调控因子，同时也是潜在的疟疾传播阻断靶点。本研究针对恶性疟原虫的不同红细胞内发育期（环状体期与裂殖体期）完成了RNA测序（RNA-seq）表达谱分析。