Involvement of salicylate and jasmonate signaling pathways in Arabidopsis interaction with Fusarium graminearum.
Involvement of salicylate and jasmonate signaling pathways in Arabidopsis interaction with Fusarium graminearum.
复制标题
DOI:
10.1094/mpmi-23-7-0861
复制
发表时间:
2010-07
期刊:
影响因子:
--
通讯作者:
Shah J
中科院分区:
文献类型:
--
作者:
Makandar R;Nalam V;Chaturvedi R;Jeannotte R;Sparks AA;Shah J
Fusarium graminearum is the principal causative agent of Fusarium head blight (FHB), a devastating disease of wheat and barley. This fungus can also colonize Arabidopsis thaliana. Disease resistance was enhanced in transgenic wheat and Arabidopsis plants that constitutively over-express the NONEXPRESSOR OF PR GENES 1 (NPR1) gene, which regulates salicylic acid (SA) signaling and modulates the activation of jasmonic acid (JA)-dependent defenses. Here, we provide several lines of evidence that reveal an important role for SA and JA signaling in Arabidopsis defense against F. graminearum. SA level was elevated in fungus-inoculated leaves and SA application and biologically activated systemic acquired resistance enhanced resistance. Furthermore, the disruption of SA accumulation and signaling in the sid2 mutant and NahG transgenic plant, and the npr1 and wrky18 mutants, respectively, resulted in heightened susceptibility to this fungus in leaves and inflorescence. JA signaling was activated in parallel with SA signaling in the fungus-challenged plants. But, the hyper-resistance of the JA pathway mutants, opr3, coi1 and jar1 indicates that this pathway contributes to susceptibility. Genetic and biochemical experiments indicate that the JA pathway promotes disease by attenuating the activation of SA signaling in fungus-inoculated plants. However, the hyper-susceptibility of the jar1 npr1 double mutant compared to the npr1 mutant suggests that JAR1 also contributes to defense, signifying a dichotomous role of JA and JAR1-dependent mechanism in this interaction.