Murray Shane L, Thomson Catherine, Chini Andrea, Read Nick D, Loake Gary J
Institute of Cell & Molecular Biology, University of Edinburgh, Scotland, UK.
Mol Plant Microbe Interact. 2002 Jun;15(6):557-66. doi: 10.1094/MPMI.2002.15.6.557.
In order to identify components of the defense signaling network engaged following attempted pathogen invasion, we generated a novel PR-1::luciferase (LUC) transgenic line that was deployed in an imaging-based screen to uncover defense-related mutants. The recessive mutant designated cir1 exhibited constitutive expression of salicylic acid (SA), jasmonic acid (JA)/ethylene, and reactive oxygen intermediate-dependent genes. Moreover, this mutation conferred resistance against the bacterial pathogen Pseudomonas syringae pv. tomato DC3000 and a virulent oomycete pathogen Peronospora parasitica Noco2. Epistasis analyses were undertaken between cir1 and mutants that disrupt the SA (nprl, nahG), JA (jar1), and ethylene (ET) (ein2) signaling pathways. While resistance against both P. syringae pv. tomato DC3000 and Peronospora parasitica Noco2 was partially reduced by npr1, resistance against both of these pathogens was lost in an nahG genetic background. Hence, cirl-mediated resistance is established via NPR1-dependent and -independent signaling pathways and SA accumulation is essential for the function of both pathways. While jar1 and ein2 reduced resistance against P. syringae pv. tomato DC3000, these mutations appeared not to impact cir1-mediated resistance against Peronospora parasitica Noco2. Thus, JA and ET sensitivity are required for cir1-mediated resistance against P. syringae pv. tomato DC3000 but not Peronospora parasitica Noco2. Therefore, the cir1 mutation may define a negative regulator of disease resistance that operates upstream of SA, JA, and ET accumulation.
为了鉴定病原体入侵尝试后参与防御信号网络的组分，我们构建了一种新型的PR-1::荧光素酶（LUC）转基因系，并将其用于基于成像的筛选以发现与防御相关的突变体。命名为cir1的隐性突变体表现出水杨酸（SA）、茉莉酸（JA）/乙烯以及活性氧中间体依赖性基因的组成型表达。此外，该突变赋予了对细菌病原体丁香假单胞菌番茄致病变种DC3000和致病卵菌病原体寄生霜霉Noco2的抗性。对cir1与破坏SA（npr1、nahG）、JA（jar1）和乙烯（ET）（ein2）信号通路的突变体进行了上位性分析。虽然npr1部分降低了对丁香假单胞菌番茄致病变种DC3000和寄生霜霉Noco2的抗性，但在nahG遗传背景下对这两种病原体的抗性均丧失。因此，cir1介导的抗性是通过依赖NPR1和不依赖NPR1的信号通路建立的，SA积累对于这两条通路的功能都是必不可少的。虽然jar1和ein2降低了对丁香假单胞菌番茄致病变种DC3000的抗性，但这些突变似乎不影响cir1介导的对寄生霜霉Noco2的抗性。因此，cir1介导的对丁香假单胞菌番茄致病变种DC3000的抗性需要JA和ET敏感性，但对寄生霜霉Noco2的抗性则不需要。因此，cir1突变可能定义了一种抗病性的负调控因子，其作用于SA, JA和ET积累的上游。
