Muller's Ratchet and Ribosome Degeneration in the Obligate Intracellular Parasites Microsporidia
Muller's Ratchet and Ribosome Degeneration in the Obligate Intracellular Parasites Microsporidia
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DOI：
10.3390/ijms19124125
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发表时间：
2018-12-01
影响因子：
5.6
通讯作者：
Soell, Dieter
中科院分区：
文献类型：
--
作者：
Melnikov, Sergey V.;Manakongtreecheep, Kasidet;Soell, Dieter
微孢子虫是真菌类寄生虫，具有已知最小的真核生物基因组，因此它们被用作研究寄生生命形式中基因组衰变现象的模型。与其他在自然选择减轻的环境中无性繁殖的细胞内寄生虫类似，微孢子虫经历了由穆勒棘轮驱动的连续基因组衰变——这是一种不可逆的有害突变积累的进化过程，导致基因丢失和细胞成分小型化。特别是，微孢子虫具有非常小的核糖体，其中rRNA被还原到最小的酶核。在这项研究中，我们分析了微孢子虫核糖体，以研究穆勒棘轮对寄生生命形式中RNA和蛋白质分子结构的明显影响。通过微孢子虫蛋白质组的质谱分析和微孢子虫基因组的分析，我们发现微孢子虫核糖体中大量的rRNA减少似乎湮灭了核糖体蛋白eL8、eL27和eS31的结合位点，这表明这些蛋白在微孢子虫物种中不再与核糖体结合。然后，我们提供了一个证据，证明蛋白eS31在微孢子虫中保留是由于其在泛素生物发生中的非核糖体功能。我们的研究表明，虽然微孢子虫携带与非寄生真核生物相同的一组核糖体蛋白，但一些核糖体蛋白在微孢子虫中不再参与蛋白质合成，并且通过具有核糖体外功能而免于基因组衰变。更普遍的是，我们的研究表明，寄生细胞的许多成分，通过病原基因组的自动注释识别，可能由于持续的基因组衰变而缺乏部分生物学功能。
Microsporidia are fungi-like parasites that have the smallest known eukaryotic genome, and for that reason they are used as a model to study the phenomenon of genome decay in parasitic forms of life. Similar to other intracellular parasites that reproduce asexually in an environment with alleviated natural selection, Microsporidia experience continuous genome decay that is driven by Muller's ratchet-an evolutionary process of irreversible accumulation of deleterious mutations that lead to gene loss and the miniaturization of cellular components. Particularly, Microsporidia have remarkably small ribosomes in which the rRNA is reduced to the minimal enzymatic core. In this study, we analyzed microsporidian ribosomes to study an apparent impact of Muller's ratchet on structure of RNA and protein molecules in parasitic forms of life. Through mass spectrometry of microsporidian proteome and analysis of microsporidian genomes, we found that massive rRNA reduction in microsporidian ribosomes appears to annihilate the binding sites for ribosomal proteins eL8, eL27, and eS31, suggesting that these proteins are no longer bound to the ribosome in microsporidian species. We then provided an evidence that protein eS31 is retained in Microsporidia due to its non-ribosomal function in ubiquitin biogenesis. Our study illustrates that, while Microsporidia carry the same set of ribosomal proteins as non-parasitic eukaryotes, some ribosomal proteins are no longer participating in protein synthesis in Microsporidia and they are preserved from genome decay by having extra-ribosomal functions. More generally, our study shows that many components of parasitic cells, which are identified by automated annotation of pathogenic genomes, may lack part of their biological functions due to continuous genome decay.