PLOS Biol:有益菌不有益,多了也致命

2015年2月12日 訊 /生物谷BIOON/ --和許多動物一樣，我們的機體中寄居著許多不同的有益細菌，這些細菌惠及宿主機體的同時也會幫助自己進行生存及擴散，但是如果細菌生長地太多就會對機體產生致命的影響，近日，一篇發表在國際雜誌PLoS Biology上的研究報導中，來自葡萄牙的研究人員通過研究發現，單一基因組的改變或許會通過增強細菌在宿主中的密度來將有益細菌轉化為有害細菌。

文章中，研究者對寄居在黑腹果蠅機體中的沃爾巴克體進行研究來揭示良性細菌如何轉變為致病細菌，沃爾巴克經常寄生於昆蟲體內保護其抵禦病毒的感染，比如登革熱病毒的侵襲等。此前研究發現，果蠅體內的沃爾巴克體的數量可以決定其對宿主的影響，而當在宿主體內達到一定的水平時沃爾巴克體就會變得非常有害，因此本文研究中研究者目的是調查控制宿主體內細菌密度的遺傳基礎。

對比了致病性和非致病性的沃爾巴克體後，研究者表示，沃爾巴克體的基因組中特殊區域的一系列重複（名為Octomom）或許是引發沃爾巴克體毒力差異的原因，而該基因組區域的拷貝數在單一果蠅機體中也是不斷變化的，攜帶更多Octomom拷貝的細菌在果蠅體內往往更容易生長達到較高密度，因此攜帶的拷貝數越多果蠅就死亡地越早，然而從另一個角度來講，攜帶更多拷貝的Octomom區域及高水平的沃爾巴克體也越容易增強果蠅機體的抗病毒能力。

Ewa Chrostek說道，我們發現Octomom的拷貝數量可以快速改變，從而引發果蠅沃爾巴克體感染的不同結果，而沃爾巴克體也會發生快速進化並且很容易破壞宿主的控制。文章中研究者發現了沃爾巴克體的基因組特殊區域可以調節其在果蠅機體中的密度，這對於後期進行更為深入的研究奠定了基礎。

當前作為有效控制登革熱傳播的方法，研究人員在野外不斷釋放感染沃爾巴克體的埃及伊蚊，因此理解沃爾巴克體的進化及種群密度控制的機制對於開發有效控制登革熱的新型預防策略也非常關鍵。（生物谷Bioon.com）

本文系生物谷原創編譯整理，歡迎轉載！轉載請註明來源並附原文連結。謝謝！

Mutualism Breakdown by Amplification of Wolbachia Genes.

Ewa Chrostek, Luis Teixeira.

Most insect species are associated with vertically transmitted endosymbionts. Because of the mode of transmission, the fitness of these symbionts is dependent on the fitness of the hosts. Therefore, these endosymbionts need to control their proliferation in order to minimize their cost for the host. The genetic bases and mechanisms of this regulation remain largely undetermined. The maternally inherited bacteria of the genus Wolbachia are the most common endosymbionts of insects, providing some of them with fitness benefits. In Drosophila melanogaster, Wolbachia wMelPop is a unique virulent variant that proliferates massively in the hosts and shortens their lifespan. The genetic bases of wMelPop virulence are unknown, and their identification would allow a better understanding of how Wolbachia levels are regulated. Here we show that amplification of a region containing eight Wolbachia genes, called Octomom, is responsible for wMelPop virulence. Using Drosophila lines selected for carrying Wolbachia with different Octomom copy numbers, we demonstrate that the number of Octomom copies determines Wolbachia titers and the strength of the lethal phenotype. Octomom amplification is unstable, and reversion of copy number to one reverts all the phenotypes. Our results provide a link between genotype and phenotype in Wolbachia and identify a genomic region regulating Wolbachia proliferation. We also prove that these bacteria can evolve rapidly. Rapid evolution by changes in gene copy number may be common in endosymbionts with a high number of mobile elements and other repeated regions. Understanding wMelPop pathogenicity and variability also allows researchers to better control and predict the outcome of releasing mosquitoes transinfected with this variant to block human vector-borne diseases. Our results show that transition from a mutualist to a pathogen may occur because of a single genomic change in the endosymbiont. This implies that there must be constant selection on endosymbionts to control their densities.