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以耐盐植物藜(Chenopodium album)为材料,利用同源克隆技术获得了7个CDPK基因核心序列,并将其命名为CaCPK1–7。随后通过RACE技术成功获得CaCPK1–3的开放阅读框(ORF)序列,其ORF分别包含长度为1 632、1 704和1 590 bp的核苷酸序列。CaCPK1–3分别编码由543、567和529个氨基酸残基组成的钙依赖型蛋白激酶。定量PCR实验显示,CaCPK1–4受盐胁迫诱导明显上调表达,随胁迫时间增加不同基因呈现各异的表达规律。对CaCPK1–3在其它非生物胁迫下的表达分析显示,CaCPK1、CaCPK2和CaCPK3的表达均受外源ABA和H2O2的调控,H2O2合成抑制剂DPI和ABA合成抑制剂Na2WO4显著抑制300 mmol·L–1NaCl处理下CaCPK1、CaCPK2和CaCPK3的表达。研究结果为揭示藜在盐胁迫信号转导过程中CDPK基因家族的功能提供了理论依据。
Using the salt-tolerant Chenopodium album as materials, seven CDPK gene core sequences were obtained by homologous cloning technology and named as CaCPK1-7. Subsequently, the open reading frame (ORF) sequence of CaCPK1-3 was successfully obtained by RACE technology, and the ORFs thereof respectively contained the nucleotide sequences of 1 632,1 704 and 1 590 bp in length. CaCPK1-3 encodes a calcium-dependent protein kinase consisting of 543, 567 and 529 amino acid residues, respectively. Quantitative PCR experiments showed that CaCPK1-4 was up-regulated by salt stress and expressed differently with different stress time. The expression analysis of CaCPK1-3 under other abiotic stresses showed that the expressions of CaCPK1, CaCPK2 and CaCPK3 were all regulated by exogenous ABA and H2O2, DPI, an inhibitor of H2O2 synthesis, and Na2WO4, an inhibitor of ABA synthesis, significantly inhibited 300 mmol·L- The expression of CaCPK1, CaCPK2 and CaCPK3 under 1NaCl treatment. The results provide a theoretical basis for revealing the function of CDPK gene family during the signal transduction of salt stress.