Functional inactivation of OsGCNT induces enhanced disease resistance to Xanthomonas oryzae pv. oryzae in rice

Abstract

BackgroundSpotted-leaf mutants are important to reveal programmed cell death and defense-related pathways in rice. We previously characterized the phenotype performance of a rice spotted-leaf mutant spl21 and narrowed down the causal gene locus spl21(t) to an 87-kb region in chromosome 12 by map-based cloning.ResultWe showed that a single base substitution from A to G at position 836 in the coding sequence of Oryza sativa beta-1,6-N-acetylglucosaminyl transferase (OsGCNT), effectively mutating Tyr to Cys at position 279 in the translated protein sequence, was responsible for the spotted-leaf phenotype as it could be rescued by functional complementation. Compared to the wild type IR64, the spotted-leaf mutant spl21 exhibited loss of chlorophyll, breakdown of chloroplasts, down-regulation of photosynthesis-related genes, and up-regulation of senescence associated genes, which indicated that OsGCNT regulates premature leaf senescence. Moreover, the enhanced resistance to the bacterial leaf blight pathogen Xanthomonas oryzae pv. oryzae, up-regulation of pathogenesis-related genes and increased level of jasmonate which suggested that OsGCNT is a negative regulator of defense response in rice. OsGCNT was expressed constitutively in the leaves, sheaths, stems, roots, and panicles, and OsGCNT-GFP was localized to the Golgi apparatus. High throughput RNA sequencing analysis provided further evidence for the biological effects of loss of OsGCNT function on cell death, premature leaf senescence and enhanced disease resistance in rice. Thus, we demonstrated that the novel OsGCNT regulated rice innate immunity and immunity-associated leaf senescence probably by changing the jasmonate metabolic pathway.ConclusionsThese results reveal that a novel gene Oryza sativa beta-1,6-N-acetylglucosaminyl transferase (OsGCNT) is responsible for the spotted-leaf mutant spl21, and OsGCNT acts as a negative-regulator mediating defense response and immunity-associated premature leaf senescence probably by activating jasmonate signaling pathway.Electronic supplementary materialThe online version of this article (10.1186/s12870-018-1489-9) contains supplementary material, which is available to authorized users.

Identification and characterization of a spotted-leaf mutant spl40 with enhanced bacterial blight resistance in rice

“…Spotted-leaf mutants often show enhanced resistance to pathogen infection along with constitutive expression of defense response genes (Yin et al 2000; Mizobuchi et al 2002; Wu et al 2008; Xu et al 2018). In a rice spl21 mutant, upregulated expression of pathogenesis-related genes and increased level of jasmonic acid leads to enhanced resistance to bacterial blight pathogen Xanthomonas oryzae pv.…”

“…In a rice spl21 mutant, upregulated expression of pathogenesis-related genes and increased level of jasmonic acid leads to enhanced resistance to bacterial blight pathogen Xanthomonas oryzae pv. oryzae (Xu et al 2018). In present study, spl40 mutant showed enhanced resistance to 14 races of this pathogen.…”

“…As every new lesion mimic mutant is providing some useful information about plant’s cope-up mechanism at molecular as well as physiological level, the hunt for novel lesion mimic mutants is expected to continue, even at greater pace and efforts. Appearance of lesions in most of the LMM is accompanied by some defense responses like production of reactive oxygen intermediates (ROIs), accumulation of phytoalexin, callose and phenolic compounds, enhanced expression of defense marker genes and elevated levels of signaling compounds like salicylic acid (Mori et al 2007; Qiao et al 2010; Chen et al 2012; Xu et al 2018). Many LMM with disease resistance phenotype showed the elevated expression of pathogenesis-related proteins like PR1, PR2, PR5, PR10, PBZ1 and PAL, which are the important components of plant defense against pathogens (Wang et al 2005; Mori et al 2007; Takahashi et al 2007; Qiao et al 2010; Chen et al 2012).…”

Mutation Types of CYP71P1 Cause Different Phenotypes of Mosaic Spot Lesion and Premature Leaf Senescence in Rice

“…In addition to the aforementioned mutants, the spl30 mutant also increased the resistance to rice blast ( Ruan et al, 2019 ), the cdr1 significantly increased rice blast resistance ( Takahashi et al, 2003 ), and the spl28 plants showed enhanced resistance to both blast and bacterial blight ( Qiao et al, 2010 ). Collectively, most of the rice LMMs show improved resistance to pathogens ( Xu et al, 2018 ; Tian et al, 2020 ).…”

LMM24 Encodes Receptor-Like Cytoplasmic Kinase 109, Which Regulates Cell Death and Defense Responses in Rice

“…Lesion mimic mutants (LMMs) display spontaneous lesions in the absence of pathogen attack, environmental stress, or mechanical damage [1], exhibiting a similar phenotype to the pathogen infection-induced hypersensitive response (HR) mediated through programmed cell death (PCD) [2]. Programmed cell death plays an important role in the innate immunity of plants by initiating the cell death process to defend against pathogen infection [3]. In fact, most LMMs show increased resistance to pathogens: The spl30 mutant shows enhanced resistance to the bacterial pathogen Xanthomonas oryzae pv oryzae ( Xoo ); dj-lm shows enhanced resistance to rice blast ( M. oryzae ) [4]; and oscul3a shows enhanced resistance to both M. oryzae and Xoo [5,6].…”