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<p>Calcium is a key component in the shell and skeleton structure, serving as a second messenger for regulating biomineralization across many species. Ocean acidification (OA) is well-studied for causing shell dissolution in marine bivalve species by disordering calcium deposition. However, the regulatory pathway of calcification affected by OA remains unclear. This study assessed eastern oyster (<i>Crassostrea virginica</i>) to determine how calcium signaling responds to elevated <i>p</i>CO<sub>2</sub> and influences shell formation. Under elevated <i>p</i>CO<sub>2</sub>, increased calcium influx was found in mantle epithelial cells, followed by the upregulation of calmodulin, a primary sensor of intracellular calcium. Expression levels of shell matrix proteins (SMPs), representing shell construction conditions, were significantly upregulated in the CO<sub>2</sub>-induced mantle cells. Larval <i>C. virginica</i> exhibited developmental stage-dependent alterations in calcium signaling and SMPs disarrangement stimulated by <i>p</i>CO<sub>2</sub>. Pharmaceutical blockage of the calcium binding on calmodulin induced abnormal expression of downstream genes and shell matrix changes consistent with those caused by elevated <i>p</i>CO<sub>2</sub>. Restored SMPs expressions in CO<sub>2</sub>-treated mantle cells were achieved by rescuing the level of calcineurin, a downstream effector of calmodulin. These findings suggest that shell deformities under OA are primarily caused by the disruption of the calcium-calmodulin signaling pathway in mantle epithelial cells.</p>

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Ocean acidification disrupts the biomineralization process in the oyster Crassostrea virginica via intracellular calcium signaling dysregulation

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年3月17日

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  • Chi Huang,
  • Joseph Matt,
  • Christopher Hollenbeck,
  • Leisha Martin,
  • Wei Xu

摘要

Calcium is a key component in the shell and skeleton structure, serving as a second messenger for regulating biomineralization across many species. Ocean acidification (OA) is well-studied for causing shell dissolution in marine bivalve species by disordering calcium deposition. However, the regulatory pathway of calcification affected by OA remains unclear. This study assessed eastern oyster (Crassostrea virginica) to determine how calcium signaling responds to elevated pCO2 and influences shell formation. Under elevated pCO2, increased calcium influx was found in mantle epithelial cells, followed by the upregulation of calmodulin, a primary sensor of intracellular calcium. Expression levels of shell matrix proteins (SMPs), representing shell construction conditions, were significantly upregulated in the CO2-induced mantle cells. Larval C. virginica exhibited developmental stage-dependent alterations in calcium signaling and SMPs disarrangement stimulated by pCO2. Pharmaceutical blockage of the calcium binding on calmodulin induced abnormal expression of downstream genes and shell matrix changes consistent with those caused by elevated pCO2. Restored SMPs expressions in CO2-treated mantle cells were achieved by rescuing the level of calcineurin, a downstream effector of calmodulin. These findings suggest that shell deformities under OA are primarily caused by the disruption of the calcium-calmodulin signaling pathway in mantle epithelial cells.