Functions of the lethal leaf-spot 1 gene in wheat cell death and disease tolerance to Puccinia striiformis.
Functions of the lethal leaf-spot 1 gene in wheat cell death and disease tolerance to Puccinia striiformis.
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致死性叶斑病1基因在小麦细胞死亡和条锈菌抗病性中的作用
DOI：
10.1093/jxb/ert135
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发表时间：
2013-07
影响因子：
6.9
通讯作者：
Kang Z
中科院分区：
文献类型：
--
作者：
Tang C;Wang X;Duan X;Wang X;Huang L;Kang Z
脱镁叶绿酸a加氧酶（PaO）是叶绿素催化剂中的一个关键酶，已知其抑制玉米和拟南芥中的细胞死亡。PaO在叶绿素降解中的催化活性已被清楚地证明，但PaO在调节细胞死亡和植物与微生物相互作用中的功能在很大程度上尚不清楚。在这项研究中，我们的特点是在小麦中的致死叶斑1基因，TaLls 1，诱导叶片中感染条锈菌f.sp.三孢（Pst）和创伤治疗的PaO同源。TaLls 1蛋白含有一个保守的Rieske [2Fe-2S]基序和一个典型的PaO的单核铁结合位点。TaLls 1的沉默病毒诱导的基因沉默在小麦中导致叶细胞死亡没有病原体的攻击，可能是由于积累的脱镁叶绿酸a（上游底物的PaO），表明TaLls 1的抑制作用，而TaLls 1的过表达也引发细胞死亡在烟草和小麦叶片，可能是由于积累的红色叶绿素分解产物（下游产品的PaO）。进一步的缺失突变体分析表明，保守的Rieske结构域，而不是铁结合位点，是必不可少的细胞死亡诱导。因此，这些结果表明TaLls 1在维持细胞内稳态以适应各种应激中的阈值，并揭示了TaLls 1在细胞死亡调节中的作用。此外，TaLls 1在小麦中的沉默并没有改变疾病的症状，但通过显着增加H2 O2的产生，提高细胞死亡的发生，并上调病程相关基因增强对Pst的耐受性。
Pheophorbide a oxygenase (PaO) is a key enzyme in chlorophyll catabolism that is known to suppress cell death in maize and Arabidopsis. The catalytic activity of PaO in chlorophyll degradation has been clearly demonstrated, but the function of PaO in the regulation of cell death and plant–microbe interactions is largely unknown. In this study, we characterized a PaO homologue in wheat of the lethal leaf-spot 1 gene, TaLls1, that was induced in leaves infected by Puccinia striiformis f.sp. tritici (Pst) and wounding treatment. The TaLls1 protein contains a conserved Rieske [2Fe-2S] motif and a mononuclear iron-binding site typical of PaOs. Silencing of TaLls1 by virus-induced gene silencing in wheat led to leaf cell death without pathogen attacks, possibly due to the accumulation of pheophorbide a (upstream substrate of PaO), indicating a suppressor role of TaLls1, while overexpression of TaLls1 also triggered cell death in both tobacco and wheat leaves, probably owing to the accumulation of the red chlorophyll catabolite (downstream product of PaO). Further deletion mutant analysis showed that the conserved Rieske domain, but not the iron-binding site, was essential for cell death induction. These results thus suggest a threshold for TaLls1 in maintaining cell homeostasis to adapt in various stresses, and shed new light on the role of TaLls1 in cell death regulation. Furthermore, silencing of TaLls1 in wheat did not change the disease symptoms but enhanced tolerance to Pst via an significant increase in H2O2 generation, elevated cell death occurrence, and upregulation of pathogenesis-related genes.
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影响因子：
2.7
作者：
OBANNI, M;HIPSKIND, J;DUNKLE, LD
通讯作者：
DUNKLE, LD
影响因子：
7.4
作者：
Gray, J;Janick-Buckner, D;Johal, GS
通讯作者：
Johal, GS
影响因子：
5.1
作者：
Gray, J;Wardzala, E;Pauli, F
通讯作者：
Pauli, F
影响因子：
4.9
作者：
Hirashima, Masumi;Tanaka, Ryouichi;Tanaka, Ayumi
通讯作者：
Tanaka, Ayumi
影响因子：
7.2
作者：
Holzberg, S;Brosio, P;Pogue, GP
通讯作者：
Pogue, GP