Characterization and Genetic Analysis of a Novel Light-Dependent Lesion Mimic Mutant, lm3, Showing Adult-Plant Resistance to Powdery Mildew in Common Wheat

Abstract

Lesion mimics (LMs) that exhibit spontaneous disease-like lesions in the absence of pathogen attack might confer enhanced plant disease resistance to a wide range of pathogens. The LM mutant, lm3 was derived from a single naturally mutated individual in the F1 population of a 3-1/Jing411 cross, backcrossed six times with 3–1 as the recurrent parent and subsequently self-pollinated twice. The leaves of young seedlings of the lm3 mutant exhibited small, discrete white lesions under natural field conditions. The lesions first appeared at the leaf tips and subsequently expanded throughout the entire leaf blade to the leaf sheath. The lesions were initiated through light intensity and day length. Histochemical staining revealed that lesion formation might reflect programmed cell death (PCD) and abnormal accumulation of reactive oxygen species (ROS). The chlorophyll content in the mutant was significantly lower than that in wildtype, and the ratio of chlorophyll a/b was increased significantly in the mutant compared with wildtype, indicating that lm3 showed impairment of the biosynthesis or degradation of chlorophyll, and that Chlorophyll b was prone to damage during lesion formation. The lm3 mutant exhibited enhanced resistance to wheat powdery mildew fungus (Blumeria graminis f. sp. tritici; Bgt) infection, which was consistent with the increased expression of seven pathogenesis-related (PR) and two wheat chemically induced (WCI) genes involved in the defense-related reaction. Genetic analysis showed that the mutation was controlled through a single partially dominant gene, which was closely linked to Xbarc203 on chromosome 3BL; this gene was delimited to a 40 Mb region between SSR3B450.37 and SSR3B492.6 using a large derived segregating population and the available Chinese Spring chromosome 3B genome sequence. Taken together, our results provide information regarding the identification of a novel wheat LM gene, which will facilitate the additional fine-mapping and cloning of the gene to understand the mechanism underlying LM initiation and disease resistance in common wheat.

5-Aminolevulinic Acid Dehydratase Gene Dosage Affects Programmed Cell Death and Immunity

“…As several lesion mimic mutants exhibit resistance to pathogen attacks, particularly to biotrophs (Mock and Grimm, 1997;Kruse et al, 1995;Molina et al, 1999;Tang et al, 2012;Wang et al, 2016), we investigated whether Ghlmm has acquired an elevated resistance to the V. dahliae infection. Infection assays showed that Ghlmm reached the resistance level of H7124, a resistant control for V. dahlia infection, while W0 was as susceptible as Jun1, a susceptible control for V. dahliae Note that the wild-type GhLMMD protein could be expressed and purified from E. coli, while no mutant GhLMMD protein was expressed after induction.…”

“…Several lesion mimic mutants have been reported in model plant Arabidopsis (Arabidopsis thaliana; Ishikawa et al, 2001;Quesada et al, 2013) as well as in cultivated crops such as maize (Zea mays; Hu et al, 1998), rice (Oryza sativa; Sun et al, 2011), and wheat (Triticum aestivum; Wang et al, 2016). Among them, about 40 genes controlling the lesion mimics have been isolated (Bruggeman et al, 2015).…”

Excessive UDPG resulting from the mutation of UAP1 causes programmed cell death by triggering reactive oxygen species accumulation and caspase‐like activity in rice

“…The constant studies of LMMs have greatly deepened our understanding of the regulatory mechanisms governing PCD, including chloroplast activity and light energy capture, sphingolipids and fatty acids, membrane trafficking, secondary messengers, and transcription control (Moeder & Yoshioka, ; Bruggeman et al ., ).In rice, multiple biochemical events and signaling pathways are involved in the progress of lesion mimics and PCD execution, including tetrapyrrole biosynthesis (Sun et al ., ), carbohydrate metabolism (Vega‐Sanchez et al ., ), ABA signal (Wang et al ., ,b,c), protein phosphorylation mediated by wall‐associated kinase (Harkenrider et al ., ) and Ser/Thr protein kinase (Takahashi et al ., ), protein ubiquitination via E3 ubiquitin ligase (Zeng et al ., ; Liu et al ., ), vesicular trafficking (Qiao et al ., ), transcription control (Yamanouchi et al ., ), RNA splicing (Chen et al ., ), and ATPase‐mediating cellular activities (Fekih et al ., ). Moreover, the lesion occurrence has been reported to be light‐dependent in different plants (Muhlenbock et al ., ; Wang et al ., ,b,c, ), showing that light is an important stimulus inducing lesion formation.…”

“…PCD is essential for plant developmental programs and response to environmental stimuli by eliminating unnecessary cells; the process is finely controlled by multiple signaling molecules such as reactive oxygen species (ROS) and various hormones (Dominguez & Cejudo, ; Petrov et al ., ; Serrano et al ., ; Van Hautegem et al ., ; Van Durme & Nowack, ). For example, the occurrence of lesions and PCD is associated with massive ROS accumulation in rice (Kojo et al ., ; Chen et al ., ), wheat (Wang et al ., ), and Arabidopsis (Chai et al ., ). Thus, LMMs are valuable materials for unraveling the signaling pathways and molecular mechanisms governing the PCD execution in plant (Moeder & Yoshioka, ).…”

Deterioration of Antioxidant Competence in Barley Lesion Mimic Mutant 194

“…In addition, the accumulation of reactive oxygen species (ROS) and the activities of ROS-related enzymes, such as superoxide dismutase (SOD) and catalase (CAT), play important roles in the formation of the lesion mimic phenotype [17,18]. For example, the light-dependent LMM, lm3, shows adult-plant resistance to powdery mildew in common wheat because of the accumulation of ROS [19]. Furthermore, the LMM, lmm6, was more resistant than the wild type (WT) to rice blast fungus Magnaporthe grisea, and had a higher accumulation of ROS and a lower SOD enzyme activity [20].…”