title: Semi-dominant mutations in the CC-NB-LRR-type R gene, NLS1, lead to constitutive activation of defense responses in rice.
abstract: In this study, we characterized the semi-dominant mutant nls1-1D (necrotic leaf sheath 1) of rice, which displays spontaneous lesions, specifically on leaf sheaths, with a developmental pattern. nls1-1D plants also exhibited constitutively activated defense responses, including extensive cell death, excess hydrogen peroxide and salicylic acid (SA) accumulation, up-regulated expressions of pathogenesis-related genes, and enhanced resistance to bacterial pathogens. Map-based cloning revealed that NLS1 encodes a typical CC-NB-LRR-type protein in rice. The nls1-1D mutation causes a S367N substitution in the non-conserved region close to the GLPL motif of the NB domain. An adjacent S366T substitution was found in another semi-dominant mutant, nls1-2D, which exhibited the same phenotypes as nls1-1D. Combined analyses of wild-type plants transformed with the mutant NLS1 gene (nls1-1D), NLS1 RNAi and over-expression transgenic lines showed that nls1-2D is allelic to nls1-1D, and both mutations may cause constitutive auto-activation of the NLS1 R protein. Further real-time PCR analysis revealed that NLS1 is expressed constitutively in an age-dependent manner. In addition, because the morphology and constitutive defense responses of nls1-1D were not suppressed by blocking SA or NPR1 transcript accumulation, we suggest that NLS1 mediates both SA and NPR1-independent defense signaling pathways in rice.
authors.affiliation: State Key Laboratory of Plant Genomics and National Center for Plant Gene Research (Beijing), Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing 100101, China.
authors.forename: Jiuyou
authors.initials: J
authors.lastname: Tang
authors.forename: Xudong
authors.initials: X
authors.lastname: Zhu
authors.forename: Yiqin
authors.initials: Y
authors.lastname: Wang
authors.forename: Linchuan
authors.initials: L
authors.lastname: Liu
authors.forename: Bo
authors.initials: B
authors.lastname: Xu
authors.forename: Feng
authors.initials: F
authors.lastname: Li
authors.forename: Jun
authors.initials: J
authors.lastname: Fang
authors.forename: Chengcai
authors.initials: C
authors.lastname: Chu
mesh_terms: D000483:Alleles; D016923:Cell Death; D002874:Chromosome Mapping; D003001:Cloning, Molecular; D018506:Gene Expression Regulation, Plant; D017343:Genes, Plant; D005816:Genetic Complementation Test; D005838:Genotype; D006861:Hydrogen Peroxide / Q000378:metabolism; D012275:Oryza / Q000235:genetics* / Q000276:immunology / Q000382:microbiology; D010641:Phenotype; D010802:Phylogeny; D010935:Plant Diseases / Q000276:immunology / Q000382:microbiology; D018515:Plant Leaves / Q000378:metabolism / Q000502:physiology; D010940:Plant Proteins / Q000235:genetics / Q000276:immunology / Q000378:metabolism*; D030821:Plants, Genetically Modified / Q000235:genetics / Q000276:immunology / Q000382:microbiology; D017354:Point Mutation; D034622:RNA Interference; D020156:Salicylic Acid / Q000378:metabolism; D017386:Sequence Homology, Amino Acid; D015398:Signal Transduction; D015854:Up-Regulation; D014974:Xanthomonas / Q000276:immunology / Q000472:pathogenicity
chemical_list: D010940:Plant Proteins; D006861:Hydrogen Peroxide; D020156:Salicylic Acid