中文摘要：

损害模仿异种(LMM ) 基因，当病原体不在时刺激损害形成，在有免疫力的反应起重要作用。在这研究，我们描绘了米饭损害模仿异种， lmm5，它显示的轻依赖者的自发的损害。另外， lmm5 植物 Magnaporthe oryzae 和 Xanthomonas oryzae pv 的测试赛跑展出了提高的抵抗到所有。由增加防卫相关的基因的表示和氢过氧化物的累积的 oryzae (Xoo ) 。基因分析证明损害模仿 lmm5 的显型被二基因， lmm5.1 和 lmm5.4 控制，它与基于地图的克隆策略被孤立。显著地， LMM5.1 和 LMM5.4 分享 97.4% 氨基酸顺序身份，并且他们各编码象蛋白质一样的真核细胞的翻译延伸因素 1A (eEF1A ) 。而且， LMM5.1 和 LMM5.4 被表示在一织物特定并且一种 indica 特定的方式分别地。另外，定序分析的高产量的 mRNA 证实基础免疫组成地在 lmm5 异种被激活。一起拿，这些结果建议相应象 eEF1A 一样基因， LMM5.1 和 LMM5.4，否定地在米饭影响房间死亡和疾病抵抗。

英文摘要：

Lesion mimic mutant（LMM） genes, stimulating lesion formation in the absence of pathogens, play significant roles in immune response. In this study, we characterized a rice lesion mimic mutant, lmm5,which displayed light-dependent spontaneous lesions. Additionally, lmm5 plants exhibited enhanced resistance to all of the tested races of Magnaporthe oryzae and Xanthomonas oryzae pv. oryzae（Xoo） by increasing the expression of defense-related genes and the accumulation of hydrogen peroxide. Genetic analysis showed that the lesion mimic phenotype of lmm5 was controlled by two genes, lmm5.1 and lmm5.4, which were isolated with a map-based cloning strategy. Remarkably, LMM5.1 and LMM5.4 share a 97.4% amino acid sequence identity, and they each encode a eukaryotic translation elongation factor 1A（e EF1A）-like protein. Besides, LMM5.1 and LMM5.4 were expressed in a tissue-specific and an indicaspecific manner, respectively. In addition, high-throughput m RNA sequencing analysis confirmed that the basal immunity was constitutively activated in the lmm5 mutant. Taken together, these results suggest that the homologous e EF1A-like genes, LMM5.1 and LMM5.4, negatively affect cell death and disease resistance in rice.