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.
Sci Rep. 2020 Apr 9;10(1):6111. doi: 10.1038/s41598-020-62963-3.
Marine bivalves secrete calcified shells to protect their soft bodies from predation and damages, which is of great importance for their survival, and for the safety of the coastal ecosystem. In recent years, larval shell formation of marine bivalves has been severely affected by ocean acidification (OA), and previous study indicated that OA might affect such process by disrupting endogenous energy metabolism. Developmental stages from trochophore to D-shape larvae are extremely important for initial shell formation in oyster since a calcified shell was formed to cover the chitin one. In the present study, metabolomic and transcriptomic approaches were employed to investigate the energy metabolism of oyster larvae during initial shell (prodissoconch I, PDI shell) formation and under experimental OA treatment. Totally 230 chemical compounds were identified from the present dataset, most of which were highly expressed in the "middle" stage (early D-shape larvae) which was critical for PDI shell formation since a calcified shell was formed to cover the chitin one. Several compounds such as glucose, glutarylcarnitine (C5), β-hydroxyisovaleroylcarnitine, 5-methylthioadenosine (MTA), myristoleate (14:1n5) and palmitoleate (16:1n7) were identified, which were involved in energy metabolic processes including amino acid oxidation, glycolysis, pentose phosphate pathway and fatty acid metabolism. In addition, mRNA expressions of genes related to protein metabolism, glycolysis, lipid degradation, calcium transport and organic matrix formation activities were significantly down-regulated upon experimental OA. These results collectively suggested that formation of the initial shell in oyster larvae required endogenous energy coming from amino acid oxidation, glycolysis, pentose phosphate pathway and fatty acid metabolism. These metabolic activities could be severely inhibited by experimental OA, which might alter the allocation of endogenous energy. Insufficient endogenous energy supply then suppressed the mobilization of calcium and resulted in a failure or delay in PDI shell formation.
海洋双壳贝类通过分泌钙化贝壳来保护其柔软的身体免受捕食和伤害，这对于它们的生存以及沿海生态系统的安全至关重要。近年来，海洋双壳贝类幼虫的壳形成受到海洋酸化（OA）的严重影响，先前的研究表明，OA 可能通过破坏内源性能量代谢来影响这个过程。在牡蛎中，从担轮幼虫到 D 形幼虫的发育阶段对于初始壳形成非常重要，因为一个钙化壳被形成以覆盖一个几丁质壳。在本研究中，采用代谢组学和转录组学方法研究了牡蛎幼虫在初始壳（原壳形 I，PDI 壳）形成过程中的能量代谢，并在实验 OA 处理下进行了研究。从本数据集共鉴定出 230 种化学物质，其中大多数在“中间”阶段（早期 D 形幼虫）高度表达，这对于 PDI 壳形成至关重要，因为一个钙化壳被形成以覆盖一个几丁质壳。鉴定出几种化合物，如葡萄糖、戊二酰肉碱（C5）、β-羟基异戊酰肉碱、5-甲基硫代腺苷（MTA）、豆蔻酸（14:1n5）和棕榈油酸（16:1n7），它们参与了能量代谢过程，包括氨基酸氧化、糖酵解、戊糖磷酸途径和脂肪酸代谢。此外，实验 OA 下与蛋白质代谢、糖酵解、脂质降解、钙转运和有机基质形成活动相关的基因的 mRNA 表达显著下调。这些结果共同表明，牡蛎幼虫初始壳的形成需要来自氨基酸氧化、糖酵解、戊糖磷酸途径和脂肪酸代谢的内源性能量。这些代谢活动可能会被实验 OA 严重抑制，从而改变内源性能量的分配。内源性能量供应不足会抑制钙的动员，导致 PDI 壳形成失败或延迟。
