SUMMARY Early electron microscopy studies revealed the elaborate cellular features that define the unique adaptations of apicomplexan parasites. Among these were bulbous rhoptry (ROP) organelles and small, dense granules (GRAs), both of which are secreted during invasion of host cells. These early morphological studies were followed by the exploration of the cellular contents of these secretory organelles, revealing them to be comprised of highly divergent protein families with few conserved domains or predicted functions. In parallel, studies on host-pathogen interactions identified many host signaling pathways that were mysteriously altered by infection. It was only with the advent of forward and reverse genetic strategies that the connections between individual parasite effectors and the specific host pathways that they targeted finally became clear. The current repertoire of parasite effectors includes ROP kinases and pseudokinases that are secreted during invasion and that block host immune pathways. Similarly, many secretory GRA proteins alter host gene expression by activating host transcription factors, through modification of chromatin, or by inducing small noncoding RNAs. These effectors highlight novel mechanisms by which T. gondii has learned to harness host signaling to favor intracellular survival and will guide future studies designed to uncover the additional complexity of this intricate host-pathogen interaction.

中文翻译：

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靶向宿主信号传导和转录的弓形虫效应子[综述]

发明内容早期的电子显微镜研究揭示了精细的细胞特征，这些特征定义了apicomplexan寄生虫的独特适应性。其中有球根眼球（ROP）细胞器和小的致密颗粒（GRAs），两者在宿主细胞侵袭过程中都被分泌出来。这些早期的形态学研究之后，探索了这些分泌细胞器的细胞内含物，发现它们由高度分化的蛋白质家族组成，几乎没有保守的结构域或预测的功能。同时，对宿主-病原体相互作用的研究确定了许多宿主信号通路，这些通路被感染神秘地改变了。只是随着正向和反向遗传策略的出现，个体寄生效应子与它们所针对的特定宿主途径之间的联系才变得清晰起来。当前的寄生效应子库包括入侵期间分泌的ROP激酶和假激酶，它们会阻断宿主的免疫途径。同样，许多分泌型GRA蛋白通过激活宿主转录因子，修饰染色质或诱导小的非编码RNA来改变宿主基因的表达。这些效应器强调了新颖的机制，通过这些机制 通过修饰染色质或诱导小的非编码RNA。这些效应器强调了新颖的机制，通过这些机制 通过修饰染色质或诱导小的非编码RNA。这些效应器强调了新颖的机制，通过这些机制刚地弓形虫已经学会利用宿主信号来促进细胞内存活，并将指导未来的研究，以揭示这种复杂的宿主-病原体相互作用的额外复杂性。