Abstract:Spotted leaf mutant belongs to a class of mutants that can produce necrotic lesions spontaneously in plants without any attack by pathogens. These mutants have no beneficial effect on plant productivity but provide a unique opportunity to study programmed cell death in plant defense responses. A novel rice spotted leaf mutant (spl30) was isolated through low-energy heavy ion irradiation. Lesion expression was sensitive to light and humidity. The spl30 mutant caused a decrease in chlorophyll and soluble protein… Show more
“…PCD was also demonstrated by a DNA laddering during lesion formation (data not shown). To confirm that ROS accompanied PCD, we performed a DAB staining assay to assess H 2 O 2 accumulation, in which a reddish-brown polymer precipitate is generated by the interaction between DAB and H 2 O 2 in the presence of peroxidase [ 61 ]. After staining, a large amount of reddish-brown precipitate was only observed at necrotic sites in the lm3 mutant leaves ( Fig 4E–4H ), and dark reddish-brown staining appeared with increasing severity of necrosis ( Fig 4F and 4H ), indicating a high level of H 2 O 2 accumulation in the lm3 mutant.…”
Section: Resultsmentioning
confidence: 99%
“…The spl30(t) lesions were induced through light, including fluorescent light, and enhanced by higher temperatures [ 22 ], whereas the lesions of the rice Oslsd1 mutant were induced at a lower temperature and under shorter duration of daylight [ 1 ]. Moreover, the expression of lesion spots in spl30 mutants is sensitive to light and humidity [ 61 ]. In the present study, no visible lesions were detected under the 0 -h photoperiod, but lesions appeared under illumination, indicating that the mutant was light dependent, similar to the LF2010A mutant [ 14 ] and the LM lines derived from the Yanzhan1/Zaosui30 cross [ 13 ].…”
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.
“…PCD was also demonstrated by a DNA laddering during lesion formation (data not shown). To confirm that ROS accompanied PCD, we performed a DAB staining assay to assess H 2 O 2 accumulation, in which a reddish-brown polymer precipitate is generated by the interaction between DAB and H 2 O 2 in the presence of peroxidase [ 61 ]. After staining, a large amount of reddish-brown precipitate was only observed at necrotic sites in the lm3 mutant leaves ( Fig 4E–4H ), and dark reddish-brown staining appeared with increasing severity of necrosis ( Fig 4F and 4H ), indicating a high level of H 2 O 2 accumulation in the lm3 mutant.…”
Section: Resultsmentioning
confidence: 99%
“…The spl30(t) lesions were induced through light, including fluorescent light, and enhanced by higher temperatures [ 22 ], whereas the lesions of the rice Oslsd1 mutant were induced at a lower temperature and under shorter duration of daylight [ 1 ]. Moreover, the expression of lesion spots in spl30 mutants is sensitive to light and humidity [ 61 ]. In the present study, no visible lesions were detected under the 0 -h photoperiod, but lesions appeared under illumination, indicating that the mutant was light dependent, similar to the LF2010A mutant [ 14 ] and the LM lines derived from the Yanzhan1/Zaosui30 cross [ 13 ].…”
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.
“…These mutants spontaneously develop localized cell death lesions resembling those caused by HR in the absence of pathogen infection, abiotic stress or mechanical damage (Xu et al , 2014). Many LMMs display significantly enhanced resistance to disease (Wang et al , 2015 a ; Wang et al , 2015 b ) and it is believed that such mutants are ideal tools for deciphering the signal pathways of PCD and defense responses in plants.…”
HighlightLoss-of-function of the rice eEF1A-like protein SPL33 causes a lesion-mimic phenotype by triggering programmed cell death, and increases disease resistance, likely through activating defense pathways.
“…The hypersensitive response (HR), a type of PCD, is the most common characteristic of plant disease resistance, which triggers rapid cell death to inhibit further invasion of pathogens in host plant tissues [ 3 ]. Lesion mimic mutants (LMMs) or the specifically termed spotted-leaf (spl) mutants in rice could produce necrotic lesions similar to that caused by HR without pathogen infection, abiotic stress or mechanical damage [ 4 ]. In fact, it has been reported that numerous rice spl mutants display significantly enhanced disease resistance to multiple pathogens [ 5 , 6 ].…”
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.
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