State Ministry of Agriculture Key Laboratory of Monitoring and Management of Crop Pathogens and Insect Pests, Nanjing Agricultural University, Nanjing 210095, China.
J Biosci. 2010 Sep;35(3):435-50. doi: 10.1007/s12038-010-0049-8.
The harpin protein HrpN Ea induces Arabidopsis resistance to the green peach aphid by activating the ethylene signalling pathway and by recruiting EIN2, an essential regulator of ethylene signalling, for a defence response in the plant. We investigated 37 ethylene-inducible Arabidopsis transcription factor genes for their effects on the activation of ethylene signalling and insect defence. Twenty-eight of the 37 genes responded to both ethylene and HrpN Ea, and showed either increased or inhibited transcription, while 18 genes showed increased transcription not only by ethylene but also by HrpN Ea. In response to HrpN Ea, transcription levels of 22 genes increased, with AtMYB44 being the most inducible, six genes had decreased transcript levels, and nine remained unchanged. When Arabidopsis mutants previously generated by mutagenicity at the 37 genes were surveyed, 24 mutants were similar to the wild type plant while four mutants were more resistant and nine mutants were more susceptible than wild type to aphid infestation. Aphid-susceptible mutants showed a greater susceptibility for atmyb15, atmyb38 and atmyb44, which were generated previously by T-DNA insertion into the exon region of AtMYB15 and the promoter regions of AtMYB38 and AtMYB44. The atmyb44 mutant was the most susceptible to aphid infestation and most compromised in induced resistance. Resistance accompanied the expression of PDF1.2, an ethylene signalling marker gene that requires EIN2 for transcription in wild type but not in atmyb15, atmyb38, and atmyb44, suggesting a disruption of ethylene signalling in the mutants. However, only atmyb44 incurred an abrogation in induced EIN2 expression, suggesting a close relationship between AtMYB44 and EIN2.
Harpin 蛋白 HrpN Ea 通过激活乙烯信号通路并招募乙烯信号通路的必需调节剂 EIN2 为植物的防御反应，诱导拟南芥对绿桃蚜产生抗性。我们研究了 37 个乙烯诱导的拟南芥转录因子基因，以了解它们对乙烯信号激活和昆虫防御的影响。37 个基因中的 28 个基因对乙烯和 HrpN Ea 都有反应，表现出转录增加或抑制，而 18 个基因不仅受乙烯而且受 HrpN Ea 诱导转录增加。对 HrpN Ea 的响应，22 个基因的转录水平增加，其中 AtMYB44 的诱导性最强，6 个基因的转录水平降低，9 个基因不变。当对先前在 37 个基因中通过诱变产生的拟南芥突变体进行调查时，24 个突变体与野生型植物相似，4 个突变体比野生型更具抗性，9 个突变体比野生型更易受蚜虫侵害。蚜虫敏感突变体对 AtMYB15、AtMYB38 和 AtMYB44 表现出更高的敏感性，这 3 个基因先前通过 T-DNA 插入 AtMYB15 的外显子区域和 AtMYB38 和 AtMYB44 的启动子区域产生。AtMYB44 突变体最易受蚜虫侵害，在诱导抗性方面受到的影响最大。抗性伴随着 PDF1.2 的表达，这是一个乙烯信号标记基因，在野生型中需要 EIN2 转录，但在 atmyb15、atmyb38 和 atmyb44 中不需要，这表明突变体中的乙烯信号被破坏。然而，只有 AtMYB44 导致诱导的 EIN2 表达中断，这表明 AtMYB44 与 EIN2 之间存在密切关系。
