Wang Jing, Ye Bangquan, Yin Junjie, Yuan Can, Zhou Xiaogang, Li Weitao, He Min, Wang Jichun, Chen Weilan, Qin Peng, Ma Bintian, Wang Yuping, Li Shigui, Chen Xuewei
Rice Research Institute, Sichuan Agricultural University at Wenjiang, Chengdu, Sichuan 611130, China; Key Laboratory of Major Crop Diseases, Sichuan Agricultural University at Wenjiang, Chengdu 611130, China.
Rice Research Institute, Sichuan Agricultural University at Wenjiang, Chengdu, Sichuan 611130, China; Key Laboratory of Major Crop Diseases, Sichuan Agricultural University at Wenjiang, Chengdu 611130, China; Collaborative Innovation Center for Hybrid Rice in Yangtze River Basin at Sichuan, Chengdu 611130, China.
Plant Physiol Biochem. 2015 Dec;97:44-51. doi: 10.1016/j.plaphy.2015.09.001. Epub 2015 Sep 12.
Plants that spontaneously produce lesion mimics or spots, without any signs of obvious adversity, such as pesticide and mechanical damage, or pathogen infection, are so-called lesion mimic mutants (lmms). In rice, many lmms exhibit enhanced resistance to pathogens, which provides a unique opportunity to uncover the molecular mechanism underlying lmms. We isolated a rice light-dependent leaf lesion mimic mutant 1 (llm1). Lesion spots appeared in the leaves of the llm1 mutant at the tillering stage. Furthermore, the mutant llm1 had similar agronomic traits to wild type rice. Trypan blue and diamiobenzidine staining analyses revealed that the lesion spot formation on the llm1 mutant was due to programmed cell death and reactive oxygen species. The chloroplasts were severely damaged in the llm1 mutant, suggesting that chloroplast damage was associated with the formation of lesion spots in llm1. More importantly, llm1 exhibited enhanced resistance to bacterial blight pathogens within increased expression of pathogenesis related genes (PRs). Using a map-based cloning approach, we delimited the LLM1 locus to a 121-kb interval between two simple sequence repeat markers, RM17470 and RM17473, on chromosome 4. We sequenced the candidate genes on the interval and found that a base mutation had substituted adenine phosphate for thymine in the last exon of LOC_Os04g52130, which led to an amino acid change (Asp(388) to Val) in the llm1 mutant. Our investigation showed that the putative coproporphyrinogen III oxidase (CPOX) encoded by LOC_Os04g52130 was produced by LLM1 and that amino acid Asp(388) was essential for CPOX function. Our study provides the basis for further investigations into the mechanism underlying lesion mimic initiation associated with LLM1.
在没有任何明显逆境迹象（如农药和机械损伤或病原体感染）的情况下自发产生类似病斑或斑点的植物，被称为类病斑突变体（lmm）。在水稻中，许多lmm对病原体表现出增强的抗性，这为揭示lmm潜在的分子机制提供了独特的机会。我们分离出了一个水稻光依赖性叶片类病斑突变体1（llm1）。llm1突变体在分蘖期叶片上出现病斑。此外，突变体llm1与野生型水稻具有相似的农艺性状。台盼蓝和二氨基联苯胺染色分析表明，llm1突变体上病斑的形成是由于程序性细胞死亡和活性氧。llm1突变体中的叶绿体严重受损，这表明叶绿体损伤与llm1中病斑的形成有关。更重要的是，llm1在病程相关基因（PRs）表达增加的情况下，对白叶枯病菌表现出增强的抗性。使用图位克隆方法，我们将LLM1基因座定位到4号染色体上两个简单序列重复标记RM17470和RM17473之间的121 kb区间。我们对该区间的候选基因进行了测序，发现LOC_Os04g52130最后一个外显子中的一个碱基突变将胸腺嘧啶替换为腺嘌呤磷酸，这导致llm1突变体中的一个氨基酸变化（Asp(388)变为Val）。我们的研究表明，由LOC_Os04g52130编码的假定的粪卟啉原III氧化酶（CPOX）是由LLM1产生的，并且氨基酸Asp(388)对CPOX功能至关重要。我们的研究为进一步研究与LLM1相关的类病斑起始机制提供了基础。
