Much of our understanding of actin-driven phenotypes in eukaryotes has come from the “yeast-to-human” opisthokont lineage and the related amoebozoa. Outside of these groups lies the genus Naegleria, which shared a common ancestor with humans >1 billion years ago and includes the “brain-eating amoeba.” Unlike nearly all other known eukaryotic cells, Naegleria amoebae lack interphase microtubules; this suggests that actin alone drives phenotypes like cell crawling and phagocytosis. Naegleria therefore represents a powerful system to probe actin-driven functions in the absence of microtubules, yet surprisingly little is known about its actin cytoskeleton. Using genomic analysis, microscopy, and molecular perturbations, we show that Naegleria encodes conserved actin nucleators and builds Arp2/3–dependent lamellar protrusions. These protrusions correlate with the capacity to migrate and eat bacteria. Because human cells also use Arp2/3–dependent lamellar protrusions for motility and phagocytosis, this work supports an evolutionarily ancient origin for these processes and establishes Naegleria as a natural model system for studying microtubule-independent cytoskeletal phenotypes.

中文翻译：

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保守的肌动蛋白机制驱动耐格里虫的微管独立运动和吞噬作用


我们对真核生物中肌动蛋白驱动的表型的大部分理解来自“从酵母到人类”的后康体谱系和相关的阿米巴虫。在这些群体之外还有耐格里阿米巴属（Naegleria），它与 3E10 亿年前的人类有共同的祖先，其中包括“食脑变形虫”。与几乎所有其他已知的真核细胞不同，阿米巴耐格里阿米巴缺乏间期微管；这表明肌动蛋白单独驱动细胞爬行和吞噬作用等表型。因此，耐格里虫代表了一个强大的系统，可以在没有微管的情况下探测肌动蛋白驱动的功能，但令人惊讶的是，人们对其肌动蛋白细胞骨架知之甚少。利用基因组分析、显微镜和分子扰动，我们发现耐格里氏耐格里虫编码保守的肌动蛋白成核剂并构建 Arp2/3 依赖性层状突起。这些突起与迁移和吞噬细菌的能力相关。由于人类细胞也使用 Arp2/3 依赖性层状突起进行运动和吞噬作用，因此这项工作支持了这些过程的进化古老起源，并将耐格氏菌建立为研究微管无关的细胞骨架表型的自然模型系统。