De novo transcriptome analysis of the mussel Perna viridis after exposure to the toxic dinoflagellate Prorocentrum lima
De novo transcriptome analysis of the mussel Perna viridis after exposure to the toxic dinoflagellate Prorocentrum lima
复制标题
贻贝接触有毒甲藻原甲藻后的从头转录组分析
DOI：
10.1016/j.ecoenv.2020.110265
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发表时间：
2020-04-01
影响因子：
6.8
通讯作者：
Yang, Wei-dong
中科院分区：
文献类型：
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作者：
Dou, Min;Jiao, Yu-hu;Yang, Wei-dong
腹泻性贝类毒素是由有害微藻产生的毒素，在双壳类软体动物体内积累，引起多种毒性反应。这些毒性作用似乎随着DSP浓度的增加和暴露时间的延长而减弱，然而，其潜在机制仍不清楚。为了探讨潜在的分子机制，进行了佩尔纳消化腺的从头转录组分析暴露于利马原甲藻后。RNA-seq分析显示，与对照组相比，利马拟青霉暴露6 h后，分别有1886个和237个基因表达上调和下调，而暴露96 h后，分别有265个和217个基因表达上调和下调。这些差异表达基因主要涉及Nrf 2信号通路、免疫应激、细胞凋亡和细胞骨架等方面。结合qPCR结果，我们推测翡翠贻贝在短期暴露过程中可能主要依靠谷胱甘肽S-转移酶（GST）和ABC转运蛋白来抵抗DSP毒素。然而，较长时间的利玛原甲藻暴露可以激活Nrf 2信号通路和凋亡抑制蛋白（inhibitors of apoptosis protein，APPI），从而减轻DSP毒素对贻贝的损伤。DSP毒素可引起贝类细胞骨架的不稳定，对贝类的免疫系统有一定的负面影响。总的来说，我们的研究结果揭示了支撑双壳贝类对抗DSP毒素的防御机制的关键分子机制和调节代谢节点，也推进了我们目前对双壳贝类防御机制的理解。
Diarrheic shellfish poisoning (DSP) toxins are produced by harmful microalgae and accumulate in bivalve mollusks, causing various toxicity. These toxic effects appear to abate with increasing DSP concentration and longer exposure time, however, the underlying mechanisms remain unclear. To explore the underlying molecular mechanisms, de novo transcriptome analysis of the digestive gland of Perna viridis was performed after Prorocentrum lima exposure. RNA-seq analysis showed that 1886 and 237 genes were up- and down-regulated, respectively after 6 h exposure to P. lima, while 265 genes were up-regulated and 217 genes were down-regulated after 96 h compared to the control. These differentially expressed genes mainly involved in Nrf2 signing pathways, immune stress, apoptosis and cytoskeleton, etc. Combined with qPCR results, we speculated that the mussel P. viridis might mainly rely on glutathione S-transferase (GST) and ABC transporters to counteract DSP toxins during short-term exposure. However, longer exposure of P. lima could activate the Nrf2 signaling pathway and inhibitors of apoptosis protein (LAP), which in turn reduced the damage of DSP toxins to the mussel. DSP toxins could induce cytoskeleton destabilization and had some negative impact on the immune system of bivalves. Collectively, our findings uncovered the crucial molecular mechanisms and the regulatory metabolic nodes that underpin the defense mechanism of bivalves against DSP toxins and also advanced our current understanding of bivalve defense mechanisms.