Division of Infectious Diseases, Boston Children's Hospital, Boston, Massachusetts, USA.
Department of Pediatrics, Harvard Medical School, Boston, Massachusetts, USA.
mSphere. 2021 Dec 22;6(6):e0089521. doi: 10.1128/msphere.00895-21. Epub 2021 Dec 8.
Plasmodium falciparum, the Apicomplexan parasite that causes the most severe form of human malaria, divides via schizogony during the asexual blood stage of its life cycle. In this method of cell division, multiple daughter cells are generated from a single schizont by segmentation. During segmentation, the basal complex forms at the basal end of the nascent daughter parasites and likely facilitates cell shape and cytokinesis. The requirement and function for each of the individual protein components within the basal complex remain largely unknown in P. falciparum. In this work, we demonstrate that the P. falciparum membrane occupation and recognition nexus repeat-containing protein 1 (PfMORN1) is not required for asexual replication. Following inducible knockout of PfMORN1, we find no detectable defect in asexual parasite morphology or replicative fitness. Plasmodium falciparum parasites cause the most severe form of human malaria. During the clinically relevant blood stage of its life cycle, the parasites divide via schizogony. In this divergent method of cell division, the components for multiple daughter cells are generated within a common cytoplasm. At the end of schizogony, segmentation partitions the organelles into invasive daughter parasites. The basal complex is a ring-shaped molecular machine that is critical for segmentation. The requirement for individual proteins within the basal complex is incompletely understood. We demonstrate that the PfMORN1 protein is dispensable for blood stage replication of P. falciparum. This result highlights important differences between parasites and Toxoplasma gondii, where the ortholog T. gondii MORN1 (TgMORN1) is required for asexual replication.
疟原虫裂殖子，引起最严重形式的人类疟疾的 Apicomplexan 寄生虫，在其生命周期的无性血阶段通过裂殖子生殖进行分裂。在这种细胞分裂方法中，多个子细胞由单个裂殖子通过分割产生。在分割过程中，基底复合物在新生子虫的基底端形成，可能有助于细胞形状和胞质分裂。在疟原虫裂殖子中，基底复合物的每个单独蛋白成分的需求和功能在很大程度上仍然未知。在这项工作中，我们证明疟原虫膜占领和识别连接重复蛋白 1（PfMORN1）在无性复制中不是必需的。在 PfMORN1 的诱导敲除后，我们发现无性寄生虫形态或复制适应性没有可检测到的缺陷。疟原虫裂殖子引起最严重形式的人类疟疾。在其生命周期的临床相关血液阶段，寄生虫通过裂殖子生殖进行分裂。在这种分歧的细胞分裂方法中，多个子细胞的成分在共同的细胞质中产生。在裂殖子生殖结束时，分割将细胞器分割成侵袭性的子虫。基底复合物是一种环形分子机器，对分割至关重要。基底复合物内单个蛋白质的需求尚不完全清楚。我们证明 PfMORN1 蛋白对于疟原虫裂殖子的血液阶段复制是可有可无的。这一结果突出了寄生虫和刚地弓形虫之间的重要差异，后者的同源物刚地弓形虫 MORN1（TgMORN1）对于无性复制是必需的。
