Deciphering the genetic basis of microcystin tolerance.

Deciphering the genetic basis of microcystin tolerance.
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解解微囊藻蛋白耐受性的遗传基础。

DOI:
10.1186/1471-2164-15-776
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发表时间:
2014-09-09
期刊:
影响因子:
4.4
通讯作者:
von Elert E
von Elert E
中科院分区:
生物学2区
文献类型:
--
作者:
Schwarzenberger A;Sadler T;Motameny S;Ben-Khalifa K;Frommolt P;Altmüller J;Konrad K;von Elert E

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蓝藻通过产生有毒的次级代谢产物,如微囊藻毒素,对淡水生态系统构成严重威胁。这些微囊藻毒素已被证明会伤害牲畜、宠物和人类,并影响生态系统的服务和功能。由于富营养化和全球变暖,蓝藻水华在世界范围内的强度和频率都在增加。然而,水蚤,浮游藻类和蓝藻的主要食草动物,已被证明能够抑制水华形成蓝藻和适应蓝藻产生微囊藻毒素。由于水蚤的基因组是最近才公布的,现在有可能阐明水蚤耐微囊藻毒素的潜在分子机制。大型蚤喂食一种能产生微囊藻毒素的蓝藻菌株或其基因工程微囊藻毒素敲除突变体。因此,有可能区分由于摄入蓝藻的影响和微囊藻毒素特别引起的影响。通过使用RNAseq,分析不同处理之间的差异表达基因,并计算受影响的KOG类别。在这里,我们表明,在水蚤的转运蛋白基因的表达调节作为一个特定的响应微囊藻毒素。随后的qPCR和饲料补充纯微囊藻毒素证实,转运蛋白基因表达的调控与几个水蚤克隆的耐受性。在这里,我们能够确定新的候选基因,特别是响应微囊藻毒素分离蓝藻的影响微囊藻毒素的影响。这些候选基因的参与耐受微囊藻毒素的相关转运蛋白基因表达的差异与克隆耐受性。因此,阻止微囊藻毒素的摄取很可能是水蚤耐受性和适应性发展的关键机制。随着明确的候选基因的可用性,未来的调查研究水蚤种群的微囊藻毒素的本地适应过程现在是可能的。本文的在线版本(doi:10.1186/1471-2164-15-776)包含补充材料,可供授权用户使用。
Cyanobacteria constitute a serious threat to freshwater ecosystems by producing toxic secondary metabolites, e.g. microcystins. These microcystins have been shown to harm livestock, pets and humans and to affect ecosystem service and functioning. Cyanobacterial blooms are increasing worldwide in intensity and frequency due to eutrophication and global warming. However, Daphnia, the main grazer of planktonic algae and cyanobacteria, has been shown to be able to suppress bloom-forming cyanobacteria and to adapt to cyanobacteria that produce microcystins. Since Daphnia’s genome was published only recently, it is now possible to elucidate the underlying molecular mechanisms of microcystin tolerance of Daphnia. Daphnia magna was fed with either a cyanobacterial strain that produces microcystins or its genetically engineered microcystin knock-out mutant. Thus, it was possible to distinguish between effects due to the ingestion of cyanobacteria and effects caused specifically by microcystins. By using RNAseq the differentially expressed genes between the different treatments were analyzed and affected KOG-categories were calculated. Here we show that the expression of transporter genes in Daphnia was regulated as a specific response to microcystins. Subsequent qPCR and dietary supplementation with pure microcystin confirmed that the regulation of transporter gene expression was correlated with the tolerance of several Daphnia clones. Here, we were able to identify new candidate genes that specifically respond to microcystins by separating cyanobacterial effects from microcystin effects. The involvement of these candidate genes in tolerance to microcystins was validated by correlating the difference in transporter gene expression with clonal tolerance. Thus, the prevention of microcystin uptake most probably constitutes a key mechanism in the development of tolerance and adaptation of Daphnia. With the availability of clear candidate genes, future investigations examining the process of local adaptation of Daphnia populations to microcystins are now possible. The online version of this article (doi:10.1186/1471-2164-15-776) contains supplementary material, which is available to authorized users.
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