Light‐Enhanced Resistance to Magnaporthe grisea Infection in the Rice Sekiguchi Lesion Mutants

Abstract

The rice sl mutant showed two types of responses to Magnaporthe grisea infection by light treatments. One was an sl‐mutant‐type response characterized by Sekiguchi lesion expression under light waves of 400–700 nm, and the other was a wild‐type response characterized by blast and/or necrotic spot lesion expression in the dark or at wavelength between 290 and 330 nm. There was a large difference in the resistance to M. grisea infection between the mutant‐ and wild‐type responses in the rice sl mutant. When the mutant‐type response was induced in the rice sl mutant, the disease resistance was enhanced relative to that in the wild‐type response. Enhanced resistance was demonstrated by two components: (a) the number of Sekiguchi lesions was reduced relative to that of blast or necrotic lesions; (b) sporulation of M. grisea was not induced in Sekiguchi lesions. The enhanced resistance was dependent on light of 400–700 nm.

Down-Regulation of Metallothionein, a Reactive Oxygen Scavenger, by the Small GTPase OsRac1 in Rice

“…The sl mutation is recessive, and the lesions are induced by many stimuli, including pathogen infection (Kiyosawa, 1970). The sl mutant is known to show enhanced hydrogen peroxide production and resistance to blast infection in a light-dependent manner (Arase et al, 2000), and these phenotypes are further enhanced by the overexpression of Pro 35S :OsRac1-19V . In this study, we found that the expression of a previously uncharacterized metallothionein gene was down-regulated in Pro 35S :OsRac1-19V-overexpressing sl cells (Fig.…”

Physical mapping of a rice lesion mimic gene, Spl1 , to a 70-kb segment of rice chromosome 12

“…Since lesion mimic mutants form necrotic spots and some exhibit resistance to pathogens, characterization of lesion mimic mutants has provided a powerful tool for the study of the molecular mechanisms of cell death and its relationship with disease resistance (Lorrain et al 2003). The light-enhanced resistance of the spl1 mutant to multiple isolates of rice blast fungus correlates with highly activated expression of several defense-related genes (Arase et al 2000;Yin et al 2000), indicating that Spl1 may be involved in disease resistance. Cloning of the Spl1 gene should therefore shed light on the mechanism of cell death and disease response.…”

“…The spl1 mutant shows resistance to multiple isolates of the blast fungus Magnaporthe grisea, and highly activated expression of several defense-related genes (Yin et al 2000). Arase et al (2000) also reported that spl1 confers lightenhanced resistance to blast fungus. Compared to the wild-type parent, when infected with M. grisea the spl1 mutant showed light-dependent accumulation of tryptamine, and increased tryptophan decarboxylase and monoamine oxidase activities to induce spl1 lesion formation.…”

Mutation in <i>OsLMS</i>, a gene encoding a protein with two double-stranded RNA binding motifs, causes lesion mimic phenotype and early senescence in rice (<i>Oryza sativa</i> L.)

“…To this effect, many LMMs have been employed in the study of various aspect of PCD such as ROS formation (Jabs et al, 1996), the Ca 2+ ion influx (Jurkowski et al, 2004), sphingolipid metabolism (Brodersen et al, 2002) and chlorophyll biosynthesis and catabolism (Ishikawa et al, 2001). However, most lesion mimic phenotypes are caused by physiological alterations regulated by environmental factors such as light (Arase et al, 2000) temperature (Noutoshi et al, 2005) and day-length (Ishikawa et al, 2001), and are not directly associated with defense responses (Liu et al, 2003). Previous studies have shown that LMM genes encode proteins that belong to various functional groups, and examples include a membrane associated protein, an ion channel protein, a zinc-finger protein, a heat stress transcription, a U-box/Armadillo repeat protein as well as components involved in the biosynthesis/metabolic pathways of fatty acids/lipids, porphyrin and phenolic compounds (Qiao et al, 2010).…”