作物学报 ›› 2013, Vol. 39 ›› Issue (02): 373-379.doi: 10.3724/SP.J.1006.2013.00373
• 研究简报 • 上一篇
吴能表,洪鸿
WU Neng-Biao,HONG Hong
摘要:
使用外加0.15 Wm-2 UV-B及不同钙效应剂处理玉米幼苗,研究细胞Ca2+信号系统对UV-B辐射下玉米幼苗光合作用的调控机理。结果表明,UV诱导的胞内Ca2+荧光增强受胞内IP3通道阻断剂肝素(Heparin)、胞内CaM活性抑制剂三氟啦嗪(TFP)抑制,降低玉米幼苗Chl a、Chl b及Chl T含量、原初光能转化效率(Fv/Fm)、PSII活性(Fv/Fo)、Hill反应活力、水分利用效率(WUE),提高胞间二氧化碳浓度(Ci),最终导致净光合速率(Pn)下降;细胞质膜钙通道阻断剂氯化镧(LaCl3)引发的此效应较小。据此提出,UV-B辐射下,玉米幼苗叶片细胞IP3动员胞内钙库释放Ca2+,调节光合色素合成、Hill反应活性、WUE,CaM介导的下游反应调节Gs,是Ca2+信号系统最终实现对Pn调控的主要机制。
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