Abstract
Disease lesion mimic (Les/les) mutants display disease-like spontaneous lesions in the absence of pathogen infection, implying the constitutive activation of defense responses. However, the genetic and biochemical bases underlying the activated defense responses in those mutants remain largely unknown. Here, we performed integrated transcriptomics and metabolomics analysis on three typical maize Les mutants Les4, Les10, and Les17 with large, medium, and small lesion size, respectively, thereby dissecting the activated defense responses at the transcriptional and metabolomic level. A total of 1,714, 4,887, and 1,625 differentially expressed genes (DEGs) were identified in Les4, Les10, and Les17, respectively. Among them, 570, 3,299, and 447 specific differentially expressed genes (SGs) were identified, implying a specific function of each LES gene. In addition, 480 common differentially expressed genes (CGs) and 42 common differentially accumulated metabolites (CMs) were identified in all Les mutants, suggesting the robust activation of shared signaling pathways. Intriguingly, substantial analysis of the CGs indicated that genes involved in the programmed cell death, defense responses, and phenylpropanoid and terpenoid biosynthesis were most commonly activated. Genes involved in photosynthetic biosynthesis, however, were generally repressed. Consistently, the dominant CMs identified were phenylpropanoids and flavonoids. In particular, lignin, the phenylpropanoid-based polymer, was significantly increased in all three mutants. These data collectively imply that transcriptional activation of defense-related gene expression; increase of phenylpropanoid, lignin, flavonoid, and terpenoid biosynthesis; and inhibition of photosynthesis are generalnatures associated with the lesion formation and constitutively activated defense responses in those mutants. Further studies on the identified SGs and CGs will shed new light on the function of each LES gene as well as the regulatory network of defense responses in maize.
Highlights
Disease lesion mimics are a class of mutants that display diseaselike spontaneous lesions in the absence of pathogen infection
Because the three mutants are maintained as heterozygotes in different background and the phenotype of lesion mimic (Les) mutants can be affected largely by genetic background according to previous report (Hoisington et al, 1982), all Les mutants from the original stock were self-pollinated for two generations, and the segregation population of the third generation was examined phenotypically and physiologically
Plant Les/les mutants show spontaneous lesion and enhanced disease resistance that are often accompanied by stunted plant growth, implying the constitutive activation of defense responses in those mutants
Summary
Disease lesion mimics are a class of mutants that display diseaselike spontaneous lesions in the absence of pathogen infection. A huge number of disease lesion mimic mutants have been found in higher plants including Arabidopsis, rice, barley, wheat, and maize (Johal et al, 1995; Lorrain et al, 2003; Rostoks et al, 2003; Gou et al, 2009; Matin et al, 2010; Tang et al, 2013) Apart from their close association with cell death in plants (Johal et al, 1995; Bruggeman et al, 2015), most of them confer enhanced resistance to diverse pathogens; disease lesion mimic mutants have become keys for deciphering cell death and defense pathways in plants (Lorrain et al, 2003). The lesion mimic line Ning7840 and lm (lesion mimic 3) have enhanced resistance to leaf rust (Puccinia triticina) and powdery mildew (Blumeria graminis f. sp. tritici), respectively (Li and Bai, 2009; Wang et al, 2016)
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