拟南芥SnRK2.2/2.3激酶参与调节镉胁迫响应的机制探究

Mechanism of SnRK2.2/2.3 kinase involved in regulating cadmium stress response in Arabidopsis thaliana

为探究拟南芥SnRK2.2和SnRK2.3基因对Cd胁迫响应的分子机制.以野生型(WT)、双突变体SnRK2.2/2.3、过表达SnRK2.2和过表达SnRK2.3的转基因植物为材料,研究SnRK2.2和SnRK2.3基因与Cd胁迫响应的关系.发现过表达两个基因可以提高拟南芥对Cd的耐受性,表现为可以减少Cd、丙二醛(MDA)及活性氧(ROS)的累积量,增加抗氧化酶CAT、POD和SOD的活性.qRT-PCR结果显示在Cd胁迫下,两种过表达植株中铁转运蛋白IRT1和转录因子FIT、bHLH038和bHLH039表达水平受到明显抑制,ABA合成相关基因AAO3和NCED3的表达量显著上调.在Cd胁迫下,两种过表达植株中ABA含量显著高于WT和双突变体.以上结果表明:拟南芥遭受Cd胁迫时,SnRK2.2和SnRK2.3基因通过下调IRT1基因表达从而减少植物对Cd的吸收,同时通过增加内源ABA含量来缓解Cd对植物的毒害.

In order to explore the molecular mechanism of Arabidopsis SnRK2.2 and SnRK2.3 genes in response to Cd stress.Wild-type(WT),double mutant SnRK2.2/2.3,overexpressing SnRK2.2 and overexpressing SnRK2.3 transgenic plants were used as materials to study the relationship between SnRK2.2 and SnRK2.3 genes and Cd stress response.The study found that the overexpression of SnRK2.2 and SnRK2.3 genes can improve the tolerance of Arabidopsis Cd,which showed that the overexpression of the two genes can reduce the accumulation of Cd,malondialdehyde(MDA)and reactive oxygen species(ROS)and increase the activities of antioxidant enzymes CAT,POD and SOD.qRTPCR results showed that under Cd stress,the expression levels of iron-regulated transporter IRT1 transcription factors FIT,bHLH038 and bHLH039 were significantly inhibited,and the expressions levels of ABA synthesis-related genes AAO3 and NCED3 were significantly up-regulated in the two overexpressed plants.Under Cd stress,the ABA content of the two overexpressed plants was significantly higher than that of the WT and double mutant.These results suggested that when Arabidopsis was under Cd stress,SnRK2.2 and SnRK2.3 genes reduced the uptake of Cd by down-regulating the expression of the IRT1 gene,and alleviated the toxicity of Cd to plants by increasing the content of endogenous ABA.