Molecular regulation of Antigenetic Variation in protists

单细胞真核生物通过一种复杂的机制表达可变的表面蛋白，这种机制使它们能够改变其表面结构，就像它们只是改变外套一样。寄生虫使用这些转换的表面涂层来逃离免疫系统或识别特定的组织。这就是慢性传染病背后的原理。尽管其强大的影响和其在寄生虫，自由生活的原生生物和真菌的进化用途，表面蛋白表达和开关的共同机制，知之甚少。在我们以前的工作中，我们使用纤毛虫草履虫作为模型细胞，发现排他性抗原表达是由小RNA控制的，其RNAi机制涉及异染色质的形成以沉默未表达的抗原。了解基因是如何变得沉默的，只会引出一个额外的问题：基因是如何逃脱沉默的？探讨这个问题可能会导致更好地了解如何消除慢性感染。我们以前的工作已经铺平了道路，以详细描述这一途径：短RNA以及相关酶的分析将澄清的同源性依赖的影响，使排他性的表面抗原的表达。

Unicellular eukaryotes express variable surface proteins via a complicated mechanism which allows them to change their surface structure as if they were simply changing a coat. Parasites use these switching surface coats to escape from the immune system or to identify specific tissues. This is the principle behind chronic infectious disease. Despite its powerful implications and its evolved use in parasites, free-living protists and fungi, the common mechanisms of surface protein expression and switching, are poorly understood. Using the ciliate Paramecium as a model cell in our previous work, we discovered that exclusive antigen expression is controlled by small RNAs in an RNAi like mechanism involving the formation of heterochromatin to silence non expressed antigens. Understanding how genes become silent only begs an additional question: how does a gene escape silencing? Answering this question could lead to a better understanding of how to dispel chronic infections. Our previous work has paved the way to characterize this pathway in detail: analysis of the short RNAs as well as the involved enzymes will clarify the homology dependent effects enabling exclusive expression of surface antigens.