Yoshioka Keiko, Moeder Wolfgang, Kang Hong-Gu, Kachroo Pradeep, Masmoudi Khaled, Berkowitz Gerald, Klessig Daniel F
Boyce Thompson Institute for Plant Research, Ithaca, New York 14853, USA.
Plant Cell. 2006 Mar;18(3):747-63. doi: 10.1105/tpc.105.038786. Epub 2006 Feb 3.
To investigate the resistance signaling pathways activated by pathogen infection, we previously identified the Arabidopsis thaliana mutant constitutive expresser of PR genes22 (cpr22), which displays constitutive activation of multiple defense responses. Here, we identify the cpr22 mutation as a 3-kb deletion that fuses two cyclic nucleotide-gated ion channel (ATCNGC)-encoding genes, ATCNGC11 and ATCNGC12, to generate a novel chimeric gene, ATCNGC11/12. Genetic, molecular, and complementation analyses suggest that ATCNGC11/12, as well as ATCNGC11 and ATCNGC12, form functional cAMP-activated ATCNGCs and that the phenotype conferred by cpr22 is attributable to the expression of ATCNGC11/12. However, because overexpression of ATCNGC12, but not ATCNGC11, suppressed the phenotype conferred by cpr22, the development of this phenotype appears to be regulated by the ratio between ATCNGC11/12 and ATCNGC12. Analysis of knockout lines revealed that both ATCNGC11 and ATCNGC12 are positive mediators of resistance against an avirulent biotype of Hyaloperonospora parasitica. Through epistatic analyses, cpr22-mediated enhanced resistance to pathogens was found to require NDR1-dependent and EDS1/PAD4-dependent pathways. In striking contrast, none of these pathways was required for cpr22-induced salicylic acid accumulation or PR-1 gene expression. These results demonstrate that NDR1, EDS1, and PAD4 mediate other resistance signaling function(s) in addition to salicylic acid and pathogenesis-related protein accumulation. Moreover, the requirement for both NDR1-dependent and EDS1/PAD4-dependent pathways for cpr22-mediated resistance suggests that these pathways are cross-regulated.
为了研究病原体感染激活的抗性信号通路，我们之前鉴定了拟南芥PR基因22组成型表达突变体（cpr22），该突变体表现出多种防御反应的组成型激活。在此，我们确定cpr22突变是一个3 kb的缺失，它将两个编码环核苷酸门控离子通道（ATCNGC）的基因ATCNGC11和ATCNGC12融合，产生一个新的嵌合基因ATCNGC11/12。遗传、分子和互补分析表明，ATCNGC11/12以及ATCNGC11和ATCNGC12形成功能性的cAMP激活的ATCNGC，并且cpr22赋予的表型归因于ATCNGC11/12的表达。然而，由于ATCNGC12的过表达而非ATCNGC11的过表达抑制了cpr22赋予的表型，该表型的产生似乎受ATCNGC11/12与ATCNGC12之间比例的调控。对敲除系的分析表明，ATCNGC11和ATCNGC12都是对寄生霜霉无毒生物型抗性的正向介导因子。通过上位性分析，发现cpr22介导的对病原体的增强抗性需要NDR1依赖性和EDS1/PAD4依赖性途径。与之形成鲜明对比的是，这些途径对于cpr22诱导的水杨酸积累或PR - 1基因表达均非必需。这些结果表明，NDR1、EDS1和PAD4除了介导水杨酸和病程相关蛋白积累外，还介导其他抗性信号功能。此外，cpr22介导的抗性对NDR1依赖性和EDS1/PAD4依赖性途径的需求表明这些途径存在交叉调控。
