Liaoning Key Laboratory of Marine Animal Immunology, Dalian Ocean University, Dalian 116023, China; Functional Laboratory of Marine Fisheries Science and Food Production Processes, Qingdao National Laboratory for Marine Science and Technology, Qingdao 266235, China; Liaoning Key Laboratory of Marine Animal Immunology and Disease Control, Dalian Ocean University, Dalian 116023, China; Dalian Key Laboratory of Aquatic Animal Disease Prevention and Control, Dalian Ocean University, Dalian 116023, China.
State Key Laboratory of Marine Resource Utilization in South China Sea, Hainan University, Haikou, Hainan, China.
Sci Total Environ. 2020 Sep 15;735:139469. doi: 10.1016/j.scitotenv.2020.139469. Epub 2020 May 18.
Ocean acidification has severely affected the initial shell formation of marine bivalves during their larval stages. In the present study, it was found that dopamine (DA) content in early D-shape larvae was significantly higher than that in trochophore and D-shape larvae, while the serotonin (5-HT) content in early D-shape larvae and D-shape larvae was obviously higher than that in trochophore. Incubation of trochophore with 5-HT or DA could accelerate the formation of calcified shell, and the treatments with selective antagonists of receptors for 5-HT and DA (Cg5-HTR-1 and CgD1DR-1) obviously inhibited the formation of calcified shells. When oyster larvae were subjected to an experimental acidified treatment (pH 7.4), the biosynthesis of 5-HT and DA was inhibited, while the mRNA expression levels of the components in TGF-β pathway were significantly up-regulated in D-shape larvae. Moreover, the phosphorylation of TIR and the translocation of smad4 were hindered upon acidification treatments, and the expression patterns of chitinase and tyrosinase were completely reverted. These results collectively suggested that monoamine neurotransmitters 5-HT and DA could modulate the initial shell formation in oyster larvae through TGF-β smad pathway by regulating the expression of tyrosinase and chitinase to guarantee the chitin synthesis for shell formation. CO-induced seawater acidification could suppress the biosynthesis of 5-HT and DA, as well as the activation of TGF-β smad pathway, which would subvert the expression patterns of chitinase and tyrosinase and cause the failure of initial shell formation in oyster early D-shape larvae.
海洋酸化严重影响了海洋双壳贝类幼虫期的初始壳形成。在本研究中，发现早期 D 形幼虫中的多巴胺（DA）含量明显高于担轮幼虫和 D 形幼虫，而早期 D 形幼虫和 D 形幼虫中的血清素（5-HT）含量明显高于担轮幼虫。用 5-HT 或 DA 孵育担轮幼虫可以加速钙化壳的形成，而 5-HT 和 DA 受体的选择性拮抗剂（Cg5-HTR-1 和 CgD1DR-1）的处理明显抑制了钙化壳的形成。当牡蛎幼虫受到实验酸化处理（pH 7.4）时，5-HT 和 DA 的生物合成受到抑制，而 TGF-β 途径中各成分的 mRNA 表达水平在 D 形幼虫中明显上调。此外，酸化处理会阻碍 TIR 的磷酸化和 smad4 的易位，并且几丁质酶和酪氨酸酶的表达模式完全逆转。这些结果共同表明，单胺神经递质 5-HT 和 DA 可以通过 TGF-β smad 途径调节牡蛎幼虫的初始壳形成，通过调节酪氨酸酶和几丁质酶的表达来保证壳形成所需的几丁质合成。CO 诱导的海水酸化会抑制 5-HT 和 DA 的生物合成以及 TGF-β smad 途径的激活，从而颠覆几丁质酶和酪氨酸酶的表达模式，导致牡蛎早期 D 形幼虫初始壳形成失败。
