Trypanosomatid parasites are infectious agents for diseases such as African sleeping sickness, Chagas disease, and leishmaniasis that threaten millions of people, mostly in the emerging world. Trypanosomes compartmentalize glycolytic enzymes to an organelle called the glycosome, a specialized peroxisome. Functionally intact glycosomes are essential for trypanosomatid viability, making glycosomal proteins as potential drug targets against trypanosomatid diseases. Peroxins (Pex), of which Pex3 is the master regulator, control glycosome biogenesis. Although Pex3 has been found throughout the eukaryota, its identity has remained stubbornly elusive in trypanosomes. We used bioinformatics predictive of protein secondary structure to identify trypanosomal Pex3. Microscopic and biochemical analyses showed trypanosomal Pex3 to be glycosomal. Interaction of Pex3 with the peroxisomal membrane protein receptor Pex19 observed for other eukaryotes is replicated by trypanosomal Pex3 and Pex19. Depletion of Pex3 leads to mislocalization of glycosomal proteins to the cytosol, reduced glycosome numbers, and trypanosomatid death. Our findings are consistent with Pex3 being an essential gene in trypanosomes.

中文翻译：

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早期作用的糖体生物蛋白 Pex3 对于锥虫的生存能力至关重要。

锥虫寄生虫是非洲昏睡病、南美锥虫病和利什曼病等疾病的传染原，威胁着数百万人，主要是在新兴世界。锥虫将糖酵解酶划分为称为糖体的细胞器，一种专门的过氧化物酶体。功能完整的糖体对于锥虫的生存能力至关重要，使糖体蛋白成为对抗锥虫疾病的潜在药物靶点。Peroxins (Pex)，其中 Pex3 是主要调节剂，控制糖体生物发生。尽管 Pex3 已在整个真核生物中被发现，但它的身份在锥虫中仍然难以捉摸。我们使用预测蛋白质二级结构的生物信息学来鉴定锥虫 Pex3。显微镜和生化分析显示锥虫 Pex3 是糖体。在其他真核生物中观察到的 Pex3 与过氧化物酶体膜蛋白受体 Pex19 的相互作用被锥虫 Pex3 和 Pex19 复制。Pex3 的消耗导致糖体蛋白错误定位于胞质溶胶、糖体数量减少和锥虫死亡。我们的发现与Pex3是锥虫的必需基因。