Key Laboratory of Aquatic Eutrophication and Control of Harmful Algal Blooms of Guangdong Higher Education Institute, China.
Key Laboratory of Aquatic Eutrophication and Control of Harmful Algal Blooms of Guangdong Higher Education Institute, China.
Ecotoxicol Environ Saf. 2020 Apr 1;192:110265. doi: 10.1016/j.ecoenv.2020.110265. Epub 2020 Feb 9.
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 (IAP), 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.
腹泻性贝类毒素(DSP)由有害藻类产生,并在双壳贝类中积累,从而导致各种毒性。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,但是其潜在机制仍不清楚。为了探索潜在的分子机制,在棕蛤(Perna viridis)暴露于利玛原甲藻(Prorocentrum lima)后,对其消化腺进行了从头转录组分析。RNA-seq 分析表明,暴露于 P. lima 6 h 后,分别有 1886 个和 237 个基因上调和下调,而与对照组相比,暴露 96 h 后分别有 265 个基因上调和 217 个基因下调。这些差异表达基因主要涉及 Nrf2 信号通路、免疫应激、细胞凋亡和细胞骨架等。结合 qPCR 结果,我们推测棕蛤主要依靠谷胱甘肽 S-转移酶(GST)和 ABC 转运体来抵抗短期暴露的 DSP 毒素。然而,较长时间的 P. lima 暴露会激活 Nrf2 信号通路和凋亡抑制蛋白(IAP),从而降低 DSP 毒素对贻贝的损害。DSP 毒素可诱导细胞骨架不稳定,并对双壳类动物的免疫系统产生一些负面影响。总的来说,我们的研究结果揭示了贝类抵御 DSP 毒素的防御机制的关键分子机制和调节代谢节点,并提高了我们对贝类防御机制的认识。