Ocean Acidification

Highlights

• Cytoplasmic pH homeostasis was critical for N. oceanica to tolerate 5% CO₂.
• The tolerant mechanisms involved multiple physiological-biochemical processes.
• H⁺-PPase was the central regulator for alleviating cytoplasmic acidification.
• avp1 overexpression improved cytoplasmic pH regulation by raising H⁺-PPase activity.

Abstract

High CO₂ tolerance microalgae screen/breeding shows the urgent research priority when applying microalgae for flue gas CO₂ sequestration. In this study, we chose the important resource microalgae Nannochloropsis oceanica as the target organism, the regulatory mechanisms of N. oceanica were elucidated under 5% and 20% high CO₂ conditions, and the function of key regulating gene avp1 encoding H⁺-PPase was further explored. The results showed N. oceanica was tolerant to the 5% CO₂ that maintained intracellular pH homeostasis, while severe cytoplasmic acidification was occurred under the 20% CO₂ condition. Integrated physiological, biochemical, and transcriptomic analysis revealed that P-ATPase and H⁺-PPase activities were enhanced at 4 h and 4 d under the 5% CO₂ condition, respectively. Concurrently, the reprogramming of organic acid metabolism and maintenance cellular energy supply additionally mitigated intracellular acidification. Further functional validation showed that overexpression of avp1 enhanced H⁺-PPase activity, increased cytoplasmic pH values, promoted pigments accumulation and growth of N. oceanica under the high CO₂ condition. Therefore, this study clarified the working mode of N. oceanica to tolerant high CO₂ and cytoplasmic acidification, and firstly timely proved the function of avp1, provided important data basis and gene candidates for the research of applying microalgae to CO₂ sequestration.

Wang Z., Zhang B., Guo L., Pan K., Zhu B., Li J., Tang X. & Zhao Y., 2026. The responding mechanisms of Nannochloropsis oceanica to high CO2 and the regulating functions of H+-PPase. Bioresource Technology 460: 135358. doi: 10.1016/j.biortech.2026.135358. Article (subscription required).