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以超表达桃(Prunus persica)SnRK1调节亚基βγ编码基因PpSnRK1βγ1的拟南芥(Arabidopsis thaliana)为试材,使用甲基紫精(MV)模拟氧化胁迫条件,探讨超表达PpSnRK1βγ1对拟南芥植株抗氧化能力的影响及响应机制。结果表明,在0.1μmol·L~(-1) MV氧化胁迫条件下,超表达植株与野生型种子的萌发和根系生长均受到抑制,但前者具有较高的萌发率和较长的主根;2~8μmol·L~(-1)MV喷施拟南芥植株叶片,超表达植株保留更多的绿色叶片。在2μmol·L~(-1)MV喷施3h后,超表达植株丙二醛(MDA)含量显著低于野生型,四种抗氧化酶过氧化氢酶(CAT)、超氧化物歧化酶(SOD)、谷胱甘肽S-转移酶(GSTs)和过氧化物酶(POD)活性均高于野生型植株,说明超表达PpSnRK1βγ1基因能提高拟南芥植株的抗氧化能力。在氧化胁迫条件下,超表达植株的SnRK1酶活性高于野生型植株,定量PCR结果显示,在超表达PpSnRK1βγ1拟南芥中,胁迫响应基因AtHSPRO1和AtHSPRO2的表达量也均较野生型植株明显升高。因此,超表达PpSnRK1βγ1能够增强拟南芥的抗氧化能力,可能是通过PpSnRK1βγ1参与HSPRO基因的表达及抗氧化酶活性调控发挥作用的。
Arabidopsis thaliana, which overexpression Prunus persica SnRK1 regulated PpSnRK1βγ1 subunit βγ gene, was used as experimental material. Methyl viologen (MV) was used to simulate the oxidative stress conditions and the effect of overexpression of PpSnRK1βγ1 on Arabidopsis thaliana Antioxidant capacity and response mechanism. The results showed that under 0.1 μmol·L -1 MV oxidative stress, the germination and root growth of over-expressed and wild-type seeds were inhibited, but the former had higher germination rate and longer main roots; 2 The leaves of Arabidopsis plants were sprayed with ~ 8μmol·L -1 MV, and overexpression plants retained more green leaves. The content of malondialdehyde (MDA) in the overexpression plants was significantly lower than that in the wild-type plants after being sprayed with 2μmol·L -1 MV for 3h, and the activities of four antioxidant enzymes catalase (CAT), superoxide dismutase SOD, GSTs and POD were higher than that of wild type plants, indicating that Overexpression of PpSnRK1βγ1 gene can enhance the antioxidant capacity of Arabidopsis plants. Under oxidative stress, the activity of SnRK1 over-expressing plants was higher than that of wild-type plants. Quantitative PCR results showed that the expression of AtHSPRO1 and AtHSPRO2 was significantly higher than that of wild-type plants in overexpression PpSnRK1βγ1 Arabidopsis high. Therefore, overexpression of PpSnRK1βγ1 enhanced the antioxidant capacity of Arabidopsis thaliana, probably through the involvement of PpSnRK1βγ1 in HSPRO gene expression and antioxidant enzyme activity regulation.