The virulence of the malaria parasite Plasmodium falciparum is due in large part to its ability to avoid immune destruction through antigenic variation. This results from changes in expression within the multicopy var gene family that encodes the surface antigen P. falciparum erythrocyte protein one (PfEMP1). Understanding the mechanisms underlying this process has been a high-profile research focus for many years. The histone methyltransferase PfSET10 was previously identified as a key enzyme required both for parasite viability and for regulating var gene expression, thus making it a prominent target for developing antimalarial intervention strategies and the subject of considerable research focus. Here, however, we show that disruption of the gene encoding PfSET10 is not lethal and has no effect on var gene expression, in sharp contrast with previously published reports. The contradictory findings highlight the importance of reevaluating previous conclusions when new technologies become available and suggest the possibility of a previously unappreciated plasticity in epigenetic gene regulation in P. falciparum.

中文翻译：

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组蛋白甲基转移酶 PfSET10 在疟疾寄生虫抗原变异中的作用：一个警示故事

疟原虫恶性疟原虫的毒力在很大程度上是由于它能够通过抗原变异避免免疫破坏。这是由编码表面抗原恶性疟原虫红细胞蛋白一 (PfEMP1)的多拷贝var基因家族中表达的变化引起的。多年来，了解这一过程背后的机制一直是备受瞩目的研究重点。该组蛋白甲基PfSET10先前识别为关键酶需要既为寄生虫生存力和用于调节无功基因表达，从而使其成为开发抗疟干预策略的重要目标和相当多的研究重点。然而，在这里，我们表明编码 PfSET10 的基因的破坏不是致命的，并且对var基因表达没有影响，这与之前发表的报告形成鲜明对比。相互矛盾的发现强调了当新技术可用时重新评估先前结论的重要性，并表明在恶性疟原虫的表观遗传基因调控中可能存在先前未被重视的可塑性。