低温胁迫对彩叶草光合作用及叶绿素荧光的影响

Effects of low temperature stress on the photosynthesis and chlorophyll fluorescence of Solenostemon scutellarioides

以3个彩叶草品种为试材,分别在2℃和5℃胁迫4 d后转入25℃进行恢复生长,研究不同低温胁迫对彩叶草光合作用和叶绿素荧光动力学参数的影响。结果表明,低温加重了光合作用的光抑制。随着低温胁迫处理时间的延长,3个品种的净光合速率(Pn)、气孔导度(Gs)和蒸腾速率(Tr)均随胁迫时间的延长而显著下降,而胞间二氧化碳浓度(Ci)呈上升趋势,说明非气孔因素是导致光合作用下降的主要因素。3个品种规律一致,但3个品种间对低温胁迫的反应存在差异。玫红绿边的Pn下降幅度最小,说明受低温的影响相对较小,而深红金边受到的影响最大。在叶绿素荧光参数方面,低温胁迫4 d后,3个品种的PSII最大光化学效率(Fv/Fm)、PSII实际光化学量子产量(ΦPSⅡ)、光化学猝灭系数(q P)均显著下降,而非光化学猝灭系数(NPQ)呈上升趋势。恢复试验中,5℃组的植株仅少量存活,而2℃组无一存活,表明2种低温胁迫所产生的光抑制已经导致光系统II结构短期内不可恢复的伤害或失活。

Three varieties were used for studing the effects of low temperature stress on the photosynthetic characteristics and chlorophyll fluorescence of Solenostemon scutellarioides after 4 d stress under 2℃ and 5℃, and recovery in 25℃. The results showed that low temperature increased the photo inhibitions of photosynthesis. With the extension of low temperature treatment time, photosynthetic rate （ Pn）, transpiration rate （Tr） and stomatal conductance （ Gs ） were decreased with the extension of low temperature treatment time, but intercellular CO2 concentration（Ci） was in- creased with the extension of low temperature treatment time. The result suggested that non-stomatal limitations were the key factors for the decrease of Pn during the 2℃ and 5℃ stress. Three varieties showed consistent rule, but the difference could be found in the response of each cultivar to the same stress, the Pn of＂ Meihonglvbian＂ decreased least while that of ＂Shenhongjinbian＂ decreased most. About the chlorophyll fluorescence, the maximal photochemical yield（Fv/Fm） decreased,the actual photochemical efficiency of system II（φPSII） and photochemical quenching co- efficient（qP） increased after 4 d stress, and the non-photochemical quenching coefficient（NPQ） showed increasing trend. A small number could recover after the elimination of 5 ℃ , while none could recover which endured 2℃ , show that the heavy photoinhibitions have led to non-recoverable harm or inactivation in the structure of PSII.