The eukaryotic cell cycle is typically divided into distinct phases with cytokinesis immediately following mitosis. To ensure proper cell division, each phase is tightly coordinated via feedback controls named checkpoints. During its asexual replication cycle, the malaria parasite Plasmodium falciparum undergoes multiple asynchronous rounds of mitosis with segregation of uncondensed chromosomes followed by nuclear division with intact nuclear envelope. The multi‐nucleated schizont is then subjected to a single round of cytokinesis that produces dozens of daughter cells called merozoites. To date, no cell cycle checkpoints have been identified that regulate the Plasmodium spp. mode of division. Here, we identify the Plasmodium homologue of the Mini‐Chromosome Maintenance Complex Binding Protein (PfMCMBP), which co‐purified with the Mini‐Chromosome Maintenance (MCM) complex, a replicative helicase required for genomic DNA replication. By conditionally depleting PfMCMBP, we disrupt nuclear morphology and parasite proliferation without causing a block in DNA replication. By immunofluorescence microscopy, we show that PfMCMBP depletion promotes the formation of mitotic spindle microtubules with extensions to more than one DNA focus and abnormal centrin distribution. Strikingly, PfMCMBP‐deficient parasites complete cytokinesis and form aneuploid merozoites with variable cellular and nuclear sizes. Our study demonstrates that the parasite lacks a robust checkpoint response to prevent cytokinesis following aberrant karyokinesis.

中文翻译：

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尽管在恶性疟原虫的无性发育过程中有异常的核运动，但微型染色体维持复合物结合蛋白的消耗仍允许胞质分裂的进展

真核细胞周期通常分为不同的阶段，有丝分裂后立即发生胞质分裂。为了确保正确的细胞分裂，每个阶段都通过称为检查点的反馈控制进行紧密协调。在其无性复制周期中，疟原虫恶性疟原虫经历了多轮异步有丝分裂，未浓缩的染色体分离，随后核分裂，核膜完整。然后对多核裂殖体进行一轮胞质分裂，产生数十个称为裂殖子的子细胞。迄今为止，尚未确定调节疟原虫属的细胞周期检查点。划分方式。在这里，我们识别疟原虫微型染色体维持复合物结合蛋白 (PfMCMBP) 的同源物，它与微型染色体维持 (MCM) 复合物（一种基因组 DNA 复制所需的复制解旋酶）共同纯化。通过有条件地消耗 PfMCMBP，我们破坏了核形态和寄生虫增殖，而不会导致 DNA 复制受阻。通过免疫荧光显微镜，我们显示 PfMCMBP 消耗促进有丝分裂纺锤体微管的形成，其延伸到多个 DNA 焦点和异常中心蛋白分布。引人注目的是，缺乏 PfMCMBP 的寄生虫完成胞质分裂并形成具有可变细胞和核大小的非整倍体裂殖子。我们的研究表明，寄生虫缺乏强有力的检查点反应来防止异常核分裂后的胞质分裂。