PBJ:中国农大赵文生研究组在水稻类病斑突变体研究中取得新进展
类病变突变体用于阐明控制植物对病原菌攻击和环境胁迫反应的机制。虽然已有数十个基因在功能上被证明参与了几个植物物种的类病变表型，但是过敏反应的分子机制尚不清楚。
本研究，从 T-DNA 插入系中鉴定出一个类似水稻病斑突变体天然疫病叶3(nbl3)。致病基因 OsNBL3编码线粒体五肽重复序列(PPR)蛋白。Nbl3突变体表现出细胞自发死亡反应和 H2O2积累，对真菌和细菌性病原菌的抗性增强。稻属。这种抗性与几个防御相关基因的上调相一致，因此，在 nbl3中诱导了防御反应。与 nbl3相比，OsNBL3的 RNA干扰表现出更强的抗病性，而过表达系的抗病性与野生型无明显差异。此外，nbl3表现出较强的耐盐性，同时几个与盐相关的标记基因上调。发现 OsNBL3主要参与线粒体基因 nad5内含子4的剪接。阻断 OsNBL3导致复合体活性降低，替代性呼吸通路升高，线粒体形态破坏。
结果表明，PPR 蛋白编码基因 OsNBL3在水稻线粒体发育和功能发育中起重要作用，它的破坏导致了水稻的类病变表型，提高了水稻的抗病性和耐盐性。
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 upregulation 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 upregulation 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 of 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.
https://doi.org/10.1111/pbi.13659
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