Entamoeba histolytica causes invasive amoebiasis, an important neglected tropical disease with a significant global health impact. The pathogenicity and survival of E. histolytica and its reptilian equivalent, Entamoeba invadens, relies on its ability to exhibit efficient motility, evade host immune responses, and exploit host resources, all of which are governed by the actin cytoskeleton remodeling. Our study demonstrates the early origin and the regulatory role of TALE homeobox protein EiHbox1 in actin‐related cellular processes. Several genes involved in different biological pathways, including actin dynamics are differentially expressed in EiHbox1 silenced cells. EiHbox1 silenced parasites showed disrupted F‐actin organization and loss of cellular polarity. EiHbox1's presence in the anterior region of migrating cells further suggests its involvement in maintaining cellular polarity. Loss of polarized morphology of EiHbox1 silenced parasites leads to altered motility from fast, directionally persistent, and highly chemotactic to slow, random, and less chemotactic, which subsequently leads to defective aggregation during encystation. EiHbox1 knockdown also resulted in a significant reduction in phagocytic capacity and poor capping response. These findings highlight the importance of EiHbox1 of E. invadens in governing cellular processes crucial for their survival, pathogenicity, and evasion of the host immune system.

中文翻译：

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祖先TALE同源框蛋白转录因子调节原生动物寄生虫内阿米巴入侵的肌动蛋白动力学和细胞活性

溶组织内阿米巴引起侵袭性阿米巴病，这是一种被忽视的重要热带疾病，对全球健康产生重大影响。致病性和生存溶组织内阿米巴和它的爬虫类等价物，入侵内阿米巴，依赖于其表现出有效运动、逃避宿主免疫反应和利用宿主资源的能力，所有这些都受到肌动蛋白细胞骨架重塑的控制。我们的研究证明了 TALE 同源盒蛋白 EiHbox1 在肌动蛋白相关细胞过程中的早期起源和调节作用。参与不同生物途径（包括肌动蛋白动力学）的多个基因在 EiHbox1 沉默细胞中存在差异表达。 EiHbox1 沉默的寄生虫表现出 F-肌动蛋白组织破坏和细胞极性丧失。 EiHbox1 在迁移细胞前部区域的存在进一步表明它参与维持细胞极性。 EiHbox1沉默寄生虫的极化形态的丧失导致运动性从快速、定向持久和高度趋化性改变为缓慢、随机和趋化性降低，随后导致包囊期间聚集缺陷。 EiHbox1 敲低还导致吞噬能力显着降低和加帽反应较差。这些发现强调了 EiHbox1 的重要性入侵肠球菌控制对其生存、致病性和逃避宿主免疫系统至关重要的细胞过程。