Chen Hui, Zhang Yunming, He Chenliu, Wang Qiang
Key Laboratory of Algal Biology, Institute of Hydrobiology, Chinese Academy of Sciences, Wuhan 430072, Hubei, China.
Plant Cell Physiol. 2014 Mar;55(3):634-44. doi: 10.1093/pcp/pcu015. Epub 2014 Jan 20.
Changes in the cytosolic Ca(2+) levels and the role of Ca(2+) signal transduction in neutral lipid synthesis in Chlorella sp. C2 under nitrogen starvation conditions were investigated. The results detected by using the scanning ion-selective electrode technique demonstrate that nitrogen starvation induced significant Ca(2+) influx across the plasma membrane into cells. Ca(2+) fluorescence imaging and flow cytometry were used to estimate the effect of this Ca(2+) influx on the generation of the Ca(2+) signal, and the results showed that the cytosolic Ca(2+) concentration increased transiently and then remained at a stable, high level when the cells were exposed to nitrogen starvation. However, the increase could be inhibited by pre-treatment with the Ca(2+) channel blockers ruthenium red, verapamil and GdCl3, indicating that both the influx of Ca(2+) from the extracellular space via Ca(2+) channels that are localized in the plasma membrane and the release of Ca(2+) from intracellular calcium storage via the internal calcium store were required for the generation and transduction of the Ca(2+) signal. During nitrogen starvation, neutral lipid synthesis in Chlorella sp. C2 in response to stress conditions was also inhibited to differing degrees by pre-treatment with the three Ca(2+) channel blockers, demonstrating the regulation of Ca(2+) via these Ca(2+) channels in neutral lipid synthesis. The results suggested that by transduction of extracellular stress signals into the cell and the regulation of the Ca(2+) signal in neutral lipid synthesis, Ca(2+) signal transduction played important roles in the response mechanism of Chlorella sp. C2 to nitrogen starvation.
研究了小球藻C2在氮饥饿条件下胞质Ca(2+)水平的变化以及Ca(2+)信号转导在中性脂质合成中的作用。利用扫描离子选择性电极技术检测的结果表明,氮饥饿诱导Ca(2+)大量跨质膜流入细胞。采用Ca(2+)荧光成像和流式细胞术评估这种Ca(2+)流入对Ca(2+)信号产生的影响,结果显示,当细胞暴露于氮饥饿条件时,胞质Ca(2+)浓度短暂升高,然后维持在稳定的高水平。然而,Ca(2+)通道阻滞剂钌红、维拉帕米和GdCl3预处理可抑制这种升高,表明质膜上定位的Ca(2+)通道介导的细胞外空间Ca(2+)流入以及细胞内钙库介导的细胞内钙释放均是Ca(2+)信号产生和转导所必需的。在氮饥饿期间,三种Ca(2+)通道阻滞剂预处理也不同程度地抑制了小球藻C2在应激条件下的中性脂质合成,表明这些Ca(2+)通道在中性脂质合成中对Ca(2+)具有调节作用。结果表明,Ca(2+)信号转导通过将细胞外应激信号转导至细胞内以及调节中性脂质合成中的Ca(2+)信号,在小球藻C2对氮饥饿的响应机制中发挥重要作用。