Abstract
Lesion mimic mutants are excellent models for research on molecular mechanisms of cell death and defense responses in rice. We identified a new rice lesion mimic mutant lmm24 from a mutant pool of indica rice cultivar “ZhongHui8015”. The LMM24 gene was identified by MutMap, and LMM24 was confirmed as a receptor-like cytoplasmic kinase 109 by amino acid sequence analysis. The lmm24 mutant displayed dark brown lesions in leaves and growth retardation that were not observed in wild-type ZH8015. The results of histochemical staining and TUNEL assays showed enhanced ROS accumulation and cell death in lmm24. Chloroplast degradation was observed in lmm24 leaves, with decreased expression of photosynthesis-related genes and increased expression of the senescence-induced STAYGREEN (SGR) gene and other senescence-associated genes. Furthermore, lmm24 exhibited enhanced resistance to rice blast fungus Magnaporthe oryzae (M. oryzae) and up-regulation of defense response genes. Our data demonstrate that LMM24 regulates cell death and defense responses in rice.
Highlights
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]
NLS1 encodes an ancient class of CC-NB-LRR-type resistance proteins, with single amino acid substitutions that lead to constitutive activation of defense responses [12]; the SPL11 gene encodes a U-Box/ARM protein, and loss of activity of this protein results in out of control PCD [13]; HPL3 encodes a hydroperoxide lyase, where loss of enzyme function reduces wound-induced green leaf volatile (GLV) emission but increases jasmonic acid (JA) accumulation, producing disease-resembling lesions spread throughout the entirety leaves [14]; and monocot-specific receptor-like kinase SDS2 positively regulates plant cell death and immunity in rice where plants over-expressing SDS2 show cell death on leaves and accumulate higher levels of ROS [15]
Expression levels of PR genes were significantly greater in lmm24 than in ZH8015 (Figure S3). These results suggested that the lmm24 mutant gene triggered a defense response to M. oryzae, which led to enhanced disease resistance asIsnot.cJi.aMteold
Summary
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]. To determine whether lmm confers higher resistance to pathogens, we employed the leaf spraying (seedling stage) and punch inoculation (tillering stage) methods to infect ZH8015 and lmm plants with the virulent M. oryzae isolate 12-144-1-1 (Figure 4A,B) Seedlings of both the mutant and ZH8015 showed susceptibility, but the morbidity rate of ZH8015 was more serious than that of the mutant. The statistical results of lesion area in the two growth stages showed that ZH8015 had significantly higher areas with lesions than the mutant (Figure 4C,D), indicating that lmm enhanced resistance to M. oryzae. Expression levels of PR genes were significantly greater in lmm than in ZH8015 (Figure S3) Together, these results suggested that the lmm mutant gene triggered a defense response to M. oryzae, which led to enhanced disease resistance asIsnot.cJi.aMteold.
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