OsNBL3, a mitochondrion‐localized pentatricopeptide repeat protein, is involved in splicing nad5 intron 4 and its disruption causes lesion mimic phenotype with enhanced resistance to biotic and abiotic stresses

• Published in: Plant biotechnology journal Vol. 19; no. 11; pp. 2277 - 2290
• Main Authors: Qiu, Tiancheng, Zhao, Xiaosheng, Feng, Huijing, Qi, Linlu, Yang, Jun, Peng, You‐Liang, Zhao, Wensheng
• Format: Journal Article
• Language: English
• Published: England John Wiley & Sons, Inc 01.11.2021; John Wiley and Sons Inc
• Subjects: Abiotic stress; Amino acids; Apoptosis; Binding sites; Blight; Cell death; Cytochrome; Deoxyribonucleic acid; Disease resistance; Disease Resistance - genetics; Disruption; DNA; Electron transport chain; Environmental stress; Gene expression; Gene Expression Regulation, Plant - genetics; Genes; Genotype & phenotype; Hydrogen peroxide; Hypersensitive response; Introns - genetics; Kinases; lesion mimic; Lesions; Magnaporthe oryzae; Mitochondria; Mitochondria - genetics; Mitochondria - metabolism; Molecular modelling; Morphology; Mutants; Mutation; nad5; Oryza - genetics; Oryza - metabolism; Oryza sativa; OsNBL3; Pathogens; pentatricopeptide repeat (PPR) protein; Phenotype; Phenotypes; Plant Diseases - genetics; Plant Proteins - genetics; Plant Proteins - metabolism; Plant species; Proteins; Rice; RNA splicing; RNA-mediated interference; salt tolerance; Salts; Senescence; Splicing; Stress, Physiological; Stresses; Xanthomonas; Xanthomonas oryzae; Oryza sativa; lesion mimic; disease resistance; pentatricopeptide repeat (PPR) protein; mitochondria; nad5; OsNBL3; salt tolerance; RNA splicing
• ISSN: 1467-7644; 1467-7652
• DOI: 10.1111/pbi.13659

Summary 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.