PBJ: OsNBL3是一种线粒体定位的五磷酸肽重复蛋白，参与了nad5内含子4的剪接，其破坏导致病变模拟表型，增强了对生物和非
病斑模拟突变体被用来阐明控制植物对病原体攻击和环境胁迫的反应的机制。虽然已有数十个基因在功能上被证明与几种植物的病损模拟表型有关，但其超敏反应的分子机制尚不清楚。
在此，从T-DNA插入系中鉴定出一个水稻(Oryza Sativa)病斑与突变体自然疫叶3(Nbl3)相似。致病基因OsNBL3编码一个线粒体定位的五肽重复(PPR)蛋白。Nbl3突变体表现出自发的细胞死亡反应和H2O2积累，对真菌和细菌病原菌稻瘟病菌和水稻白叶枯病菌表现出较强的抗性。米饭。这种抗性与几个防御相关基因的上调是一致的，因此在nbl3中诱导了防御反应。OsNBL3的RNA干扰系表现出与nbl3相似的抗病性，而高表达系的抗病性与野生型没有差异。此外，nbl3表现出更好的耐盐性，同时伴随着几个与盐相关的标记基因的上调。OsNBL3主要参与线粒体基因nad5内含子4的剪接。OsNBL3的破坏导致复合体I活性降低，交替呼吸途径增加，线粒体形态遭到破坏。
总之，这些结果表明PPR蛋白编码基因OsNBL3对线粒体的发育和功能是必不可少的，它的破坏导致了水稻类似病斑的表型，并增强了水稻的抗病和耐盐性。
Lesion mimic mutants are used to elucidate mechanisms controlling plant responses to pathogen attacks and environmental stresses. Although dozens of genes had been functionally demonstrated to be involved in lesion mimic phenotype in several plant species, the molecular mechanisms underlying the hypersensitive response are largely unknown. Here, a rice (Oryza sativa) lesion mimic mutant natural blight leaf 3 (nbl3) was identified from T-DNA insertion lines. The causative gene, OsNBL3, encodes a mitochondrion-localized pentatricopeptide repeat (PPR) protein. The nbl3 mutant exhibited spontaneous cell death response and H2O2 accumulation, and displayed enhanced resistance to the fungal and bacterial pathogens Magnaporthe oryzae and Xanthomonas oryzae pv. oryzae. This resistance was consistent with the up-regulation of several defence-related genes; thus, defence responses were induced in nbl3. RNA interference lines of OsNBL3 exhibited enhanced disease resistance similar to that of nbl3, while the disease resistance in overexpression lines did not differ from that of the wild type. In addition, nbl3 displayed improved tolerance to salt, accompanied by up-regulation of several salt-associated marker genes. OsNBL3 was found to mainly participate in the splicing of mitochondrial gene nad5 intron 4. Disruption of OsNBL3 leads to the reduction in complex I activity, the elevation of alternative respiratory pathways and the destruction of mitochondrial morphology. Overall, the results demonstrated that the PPR protein-coding gene OsNBL3 is essential for mitochondrial development and functions, and its disruption causes the lesion mimic phenotype and enhances disease resistance and tolerance to salt in rice.
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