scholarly journals Disruption of OsPHD1, Encoding a UDP-Glucose Epimerase, Causes JA Accumulation and Enhanced Bacterial Blight Resistance in Rice

2022 ◽  
Vol 23 (2) ◽  
pp. 751
Author(s):  
Yu Gao ◽  
Xiaojiao Xiang ◽  
Yingxin Zhang ◽  
Yongrun Cao ◽  
Beifang Wang ◽  
...  
Keyword(s):  
Cell Death ◽  
Defense Response ◽  
Bacterial Blight ◽  
Defense Responses ◽  
Wild Type ◽  
Causal Gene ◽  
Physiological Mechanisms ◽  
Lesion Mimic ◽  
Cloning Strategy ◽  
Ja Signaling

Lesion mimic mutants (LMMs) have been widely used in experiments in recent years for studying plant physiological mechanisms underlying programmed cell death (PCD) and defense responses. Here, we identified a lesion mimic mutant, lm212-1, which cloned the causal gene by a map-based cloning strategy, and verified this by complementation. The causal gene, OsPHD1, encodes a UDP-glucose epimerase (UGE), and the OsPHD1 was located in the chloroplast. OsPHD1 was constitutively expressed in all organs, with higher expression in leaves and other green tissues. lm212-1 exhibited decreased chlorophyll content, and the chloroplast structure was destroyed. Histochemistry results indicated that H2O2 is highly accumulated and cell death is occurred around the lesions in lm212-1. Compared to the wild type, expression levels of defense-related genes were up-regulated, and resistance to bacterial pathogens Xanthomonas oryzae pv. oryzae (Xoo) was enhanced, indicating that the defense response was activated in lm212-1, ROS production was induced by flg22, and chitin treatment also showed the same result. Jasmonic acid (JA) and methyl jasmonate (MeJA) increased, and the JA signaling pathways appeared to be disordered in lm212-1. Additionally, the overexpression lines showed the same phenotype as the wild type. Overall, our findings demonstrate that OsPHD1 is involved in the regulation of PCD and defense response in rice.

scholarly journals OsPG1 encodes a polygalacturonase that determines cell wall architecture and affects resistance to bacterial blight pathogen in rice

2021 ◽  
Author(s):  
Yongrun Cao ◽  
Yue Zhang ◽  
Yuyu Chen ◽  
Ning Yu ◽  
Shah Liaqat ◽  
...  
Keyword(s):  
Cell Death ◽  
Cell Wall ◽  
Defense Response ◽  
Cell Walls ◽  
Bacterial Blight ◽  
Defense Responses ◽  
Base Substitution ◽  
Loss Of Function ◽  
Wild Type ◽  
Bacterial Blight Pathogen

Abstract Background: Plant cell walls are the main physical barrier encountered by pathogens colonizing plant tissues. Alteration of cell wall integrity (CWI) can activate specific defenses by impairing proteins involved in cell wall biosynthesis, degradation and remodeling, or cell wall damage due to biotic or abiotic stress. Polygalacturonase (PG) depolymerize pectin by hydrolysis, thereby altering pectin composition and structures and activating cell wall defense. Although many studies of CWI have been reported, the mechanism of how PGs regulate cell wall immune response is not well understood. Results: Necrosis appeared in leaf tips at the tillering stage, finally resulting in 3-5 cm of dark brown necrotic tissue. ltn-212 showed obvious cell death and accumulation of H2O2 in leaf tips. The defense responses were activated in ltn-212 to resist bacterial blight pathogen of rice. Map based cloning revealed that a single base substitution (G-A) in the first intron caused incorrect splicing of OsPG1, resulting in a necrotic phenotype. OsPG1 is constitutively expressed in all organs, and the wild-type phenotype was restored in complementation individuals and knockout of wild-type lines resulted in necrosis as in ltn-212. Transmission electron microscopy showed that thicknesses of cell walls were significantly reduced and cell size and shape were significantly diminished in ltn-212.Conclusion: These results demonstrate that OsPG1 encodes a PG in response to the leaf tip necrosis phenotype of ltn-212. Loss-of-function mutation of ltn-212 destroyed CWI, resulting in spontaneous cell death and an auto-activated defense response including reactive oxygen species (ROS) burst and pathogenesis-related (PR) gene expression, as well as enhanced resistance to Xanthomonas oryzae pv. oryzae (Xoo). These findings promote our understanding of the CWI mediated defense response.

scholarly journals OsPG1 encodes a polygalacturonase that determines cell wall architecture and affects resistance to bacterial blight pathogen in rice

2020 ◽  
Author(s):  
Qunen Liu ◽  
Yongrun Cao ◽  
Yue Zhang ◽  
Yuyu Chen ◽  
Ning Yu ◽  
...  
Keyword(s):  
Cell Death ◽  
Cell Wall ◽  
Defense Response ◽  
Cell Walls ◽  
Bacterial Blight ◽  
Defense Responses ◽  
Base Substitution ◽  
Loss Of Function ◽  
Wild Type ◽  
Bacterial Blight Pathogen

Abstract Background Plant cell walls are the main physical barrier encountered by pathogens colonizing plant tissues. Alteration of cell wall integrity (CWI) can activate specific defenses by impairing proteins involved in cell wall biosynthesis, degradation and remodeling, or cell wall damage due to biotic or abiotic stress. Polygalacturonase (PG) depolymerize pectin by hydrolysis, thereby altering pectin composition and structures and activating cell wall defense. Although many studies of CWI have been reported, the mechanism of how PGs regulate cell wall immune response is not well understood.Results Necrosis appeared in leaf tips at the tillering stage, finally resulting in 3–5 cm of dark brown necrotic tissue. ltn-212 showed obvious cell death and accumulation of H2O2 in leaf tips. The defense responses were activated in ltn-212 to resist bacterial blight pathogen of rice. Map based cloning revealed that a single base substitution (G-A) in the first intron caused incorrect splicing of OsPG1, resulting in a necrotic phenotype. OsPG1 is constitutively expressed in all organs, and the wild-type phenotype was restored in complementation individuals and knockout of wild-type lines resulted in necrosis as in ltn-212. Transmission electron microscopy showed that thicknesses of cell walls were significantly reduced and cell size and shape were significantly diminished in ltn-212.Conclusion These results demonstrate that OsPG1 encodes a PG in response to the leaf tip necrosis phenotype of ltn-212. Loss-of-function mutation of ltn-212 destroyed CWI, resulting in spontaneous cell death and an auto-activated defense response including reactive oxygen species (ROS) burst and pathogenesis-related (PR) gene expression, as well as enhanced resistance to Xanthomonas oryzae pv. oryzae (Xoo). These findings promote our understanding of the CWI mediated defense response.

scholarly journals OsPG1 Encodes a Polygalacturonase that Determines Cell Wall Architecture and Affects Resistance to Bacterial Blight Pathogen in Rice

Rice ◽  
2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Yongrun Cao ◽  
Yue Zhang ◽  
Yuyu Chen ◽  
Ning Yu ◽  
Shah Liaqat ◽  
...  
Keyword(s):  
Cell Death ◽  
Cell Wall ◽  
Defense Response ◽  
Cell Walls ◽  
Bacterial Blight ◽  
Defense Responses ◽  
Base Substitution ◽  
Loss Of Function ◽  
Wild Type ◽  
Bacterial Blight Pathogen

Abstract Background Plant cell walls are the main physical barrier encountered by pathogens colonizing plant tissues. Alteration of cell wall integrity (CWI) can activate specific defenses by impairing proteins involved in cell wall biosynthesis, degradation and remodeling, or cell wall damage due to biotic or abiotic stress. Polygalacturonase (PG) depolymerize pectin by hydrolysis, thereby altering pectin composition and structures and activating cell wall defense. Although many studies of CWI have been reported, the mechanism of how PGs regulate cell wall immune response is not well understood. Results Necrosis appeared in leaf tips at the tillering stage, finally resulting in 3–5 cm of dark brown necrotic tissue. ltn-212 showed obvious cell death and accumulation of H2O2 in leaf tips. The defense responses were activated in ltn-212 to resist bacterial blight pathogen of rice. Map based cloning revealed that a single base substitution (G-A) in the first intron caused incorrect splicing of OsPG1, resulting in a necrotic phenotype. OsPG1 is constitutively expressed in all organs, and the wild-type phenotype was restored in complementation individuals and knockout of wild-type lines resulted in necrosis as in ltn-212. Transmission electron microscopy showed that thicknesses of cell walls were significantly reduced and cell size and shape were significantly diminished in ltn-212. Conclusion These results demonstrate that OsPG1 encodes a PG in response to the leaf tip necrosis phenotype of ltn-212. Loss-of-function mutation of ltn-212 destroyed CWI, resulting in spontaneous cell death and an auto-activated defense response including reactive oxygen species (ROS) burst and pathogenesis-related (PR) gene expression, as well as enhanced resistance to Xanthomonas oryzae pv. oryzae (Xoo). These findings promote our understanding of the CWI mediated defense response.

scholarly journals SPL36 Encodes a Receptor-like Protein Kinase that Regulates Programmed Cell Death and Defense Responses in Rice

Rice ◽  
2021 ◽  
Vol 14 (1) ◽  
Author(s):  
R. A. O. Yuchun ◽  
J. I. A. O. Ran ◽  
W. A. N. G. Sheng ◽  
W. U. Xianmei ◽  
Y. E. Hanfei ◽  
...  
Keyword(s):  
Cell Death ◽  
Salt Stress ◽  
Protein Kinase ◽  
Programmed Cell Death ◽  
Stress Responses ◽  
Defense Responses ◽  
Base Substitution ◽  
Wild Type ◽  
Salt Stress Response ◽  
Lesion Mimic

AbstractLesion mimic mutants spontaneously produce disease spots in the absence of biotic or abiotic stresses. Analyzing lesion mimic mutants’ sheds light on the mechanisms underlying programmed cell death and defense-related responses in plants. Here, we isolated and characterized the rice (Oryza sativa) spotted leaf 36 (spl36) mutant, which was identified from an ethyl methanesulfonate-mutagenized japonica cultivar Yundao population. spl36 displayed spontaneous cell death and enhanced resistance to rice bacterial pathogens. Gene expression analysis suggested that spl36 functions in the disease response by upregulating the expression of defense-related genes. Physiological and biochemical experiments indicated that more cell death occurred in spl36 than the wild type and that plant growth and development were affected in this mutant. We isolated SPL36 by map-based cloning. A single base substitution was detected in spl36, which results in a cysteine-to-arginine substitution in SPL36. SPL36 is predicted to encode a receptor-like protein kinase containing leucine-rich domains that may be involved in stress responses in rice. spl36 was more sensitive to salt stress than the wild type, suggesting that SPL36 also negatively regulates the salt-stress response. These findings suggest that SPL36 regulates the disease resistance response in rice by affecting the expression of defense- and stress-related genes.

scholarly journals Proteome Analysis of Programmed Cell Death and Defense Signaling Using the Rice Lesion Mimic Mutant cdr2

2005 ◽  
Vol 18 (1) ◽  
pp. 52-59 ◽  
Author(s):  
Hajime Tsunezuka ◽  
Masayuki Fujiwara ◽  
Tsutomu Kawasaki ◽  
Ko Shimamoto
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Proteome Analysis ◽  
Defense Responses ◽  
Spectrometric Analysis ◽  
Wild Type ◽  
High Accumulation ◽  
Defense Signaling ◽  
Lesion Mimic ◽  
Related Proteins

We have previously identified three lesion-mimic mutants, cell death and resistance (cdr), in rice. These mutants induce a series of defense responses, including expression of defense-related genes and high accumulation of phytoalexins, indicating that the cdr mutants are useful materials to study programmed cell death and defense signaling in rice. Here, we carried out a proteome analysis of the cdr2 mutant. Total proteins prepared from the wild type and the cdr2 mutant at three different stages of lesion formation were compared using two-dimensional electrophoresis. We found a total of 37 proteins that were differentially expressed between cdr2 and wild type. Among them, 28 spots were up-regulated and nine were down-regulated in the cdr2 mutant. All the protein spots were identified by mass spectrometric analysis. These differentially regulated proteins included defense-related proteins. In addition, 27 proteins were classified as metabolic enzymes, suggesting that the programmed cell death that occurs in the cdr2 mutant is associated with active metabolic changes. Our study shows that proteome analysis is a useful approach to study programmed cell death and defense signaling in plants.

scholarly journals Deletion of the SACPD-C Locus Alters the Symbiotic Relationship Between Bradyrhizobium japonicum USDA110 and Soybean, Resulting in Elicitation of Plant Defense Response and Nodulation Defects

2016 ◽  
Vol 29 (11) ◽  
pp. 862-877 ◽  
Author(s):  
Hari B. Krishnan ◽  
Alaa A. Alaswad ◽  
Nathan W. Oehrle ◽  
Jason D. Gillman
Keyword(s):  
Plant Defense ◽  
Defense Response ◽  
Acyl Carrier Protein ◽  
Defense Responses ◽  
Nodule Development ◽  
Plant Defense Response ◽  
Wild Type ◽  
Two Dimensional Gel Electrophoresis ◽  
Symbiotic Associations ◽  
Soybean Nodule

Legumes form symbiotic associations with soil-dwelling bacteria collectively called rhizobia. This association results in the formation of nodules, unique plant-derived organs, within which the rhizobia are housed. Rhizobia-encoded nitrogenase facilitates the conversion of atmospheric nitrogen into ammonia, which is utilized by the plants for its growth and development. Fatty acids have been shown to play an important role in root nodule symbiosis. In this study, we have investigated the role of stearoyl-acyl carrier protein desaturase isoform C (SACPD-C), a soybean enzyme that catalyzes the conversion of stearic acid into oleic acid, which is expressed in developing seeds and in nitrogen-fixing nodules. In-depth cytological investigation of nodule development in sacpd-c mutant lines M25 and MM106 revealed gross anatomical alteration in the sacpd-c mutants. Transmission electron microscopy observations revealed ultrastructural alterations in the sacpd-c mutants that are typically associated with plant defense response to pathogens. In nodules of two sacpd-c mutants, the combined jasmonic acid (JA) species (JA and the isoleucine conjugate of JA) were found to be reduced and 12-oxophytodienoic acid (OPDA) levels were significantly higher relative to wild-type lines. Salicylic acid levels were not significantly different between genotypes, which is divergent from previous studies of sacpd mutant studies on vegetative tissues. Soybean nodule phytohormone profiles were very divergent from those of roots, and root profiles were found to be almost identical between mutant and wild-type genotypes. The activities of antioxidant enzymes, ascorbate peroxidase, and superoxide dismutase were also found to be higher in nodules of sacpd-c mutants. PR-1 gene expression was extremely elevated in M25 and MM106, while the expression of nitrogenase was significantly reduced in these sacpd-c mutants, compared with the parent ‘Bay’. Two-dimensional gel electrophoresis and matrix-assisted laser desorption-ionization time of flight mass spectrometry analyses confirmed sacpd-c mutants also accumulated higher amounts of pathogenesis-related proteins in the nodules. Our study establishes a major role for SACPD-C activity as essential for proper maintenance of soybean nodule morphology and physiology and indicates that OPDA signaling is likely to be involved in attenuation of nodule biotic defense responses.

scholarly journals LMM24 Encodes Receptor-Like Cytoplasmic Kinase 109, Which Regulates Cell Death and Defense Responses in Rice

2019 ◽  
Vol 20 (13) ◽  
pp. 3243 ◽  
Author(s):  
Yue Zhang ◽  
Qunen Liu ◽  
Yingxin Zhang ◽  
Yuyu Chen ◽  
Ning Yu ◽  
...  
Keyword(s):  
Cell Death ◽  
Molecular Mechanisms ◽  
Indica Rice ◽  
Defense Responses ◽  
Rice Cultivar ◽  
Histochemical Staining ◽  
Lesion Mimic ◽  
Ros Accumulation ◽  
Mutant Pool ◽  
Defense Response Genes

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.

scholarly journals Arabidopsis EDR1 Protein Kinase Regulates the Association of EDS1 and PAD4 to Inhibit Cell Death

2020 ◽  
Vol 33 (4) ◽  
pp. 693-703 ◽  
Author(s):  
Matthew Neubauer ◽  
Irene Serrano ◽  
Natalie Rodibaugh ◽  
Deepak D. Bhandari ◽  
Jaqueline Bautor ◽  
...  
Keyword(s):  
Cell Death ◽  
Protein Kinase ◽  
Defense Responses ◽  
Loss Of Function ◽  
Wild Type ◽  
Independent Function ◽  
Signaling Function ◽  
Golovinomyces Cichoracearum ◽  
Powdery Mildew Pathogen ◽  
Heteromeric Association

ENHANCED DISEASE SUSCEPTIBILITY1 (EDS1) and PHYTOALEXIN DEFICIENT4 (PAD4) are sequence-related lipase-like proteins that function as a complex to regulate defense responses in Arabidopsis by both salicylic acid–dependent and independent pathways. Here, we describe a gain-of-function mutation in PAD4 (S135F) that enhances resistance and cell death in response to infection by the powdery mildew pathogen Golovinomyces cichoracearum. The mutant PAD4 protein accumulates to wild-type levels in Arabidopsis cells, thus these phenotypes are unlikely to be due to PAD4 over accumulation. The phenotypes are similar to loss-of-function mutations in the protein kinase EDR1 (Enhanced Disease Resistance1), and previous work has shown that loss of PAD4 or EDS1 suppresses edr1-mediated phenotypes, placing these proteins downstream of EDR1. Here, we show that EDR1 directly associates with EDS1 and PAD4 and inhibits their interaction in yeast and plant cells. We propose a model whereby EDR1 negatively regulates defense responses by interfering with the heteromeric association of EDS1 and PAD4. Our data indicate that the S135F mutation likely alters an EDS1-independent function of PAD4, potentially shedding light on a yet-unknown PAD4 signaling function.

scholarly journals Investigating Proteome and Transcriptome Defense Response of Apples Induced by Yarrowia lipolytica

2017 ◽  
Vol 30 (4) ◽  
pp. 301-311 ◽  
Author(s):  
Hongyin Zhang ◽  
Liangliang Chen ◽  
Yiwen Sun ◽  
Lina Zhao ◽  
Xiangfeng Zheng ◽  
...  
Keyword(s):  
Biological Control ◽  
Yarrowia Lipolytica ◽  
Stress Responses ◽  
Defense Response ◽  
Defense Responses ◽  
Penicillium Expansum ◽  
Signal Pathways ◽  
Successful Implementation ◽  
Oxidase Gene ◽  
Ja Signaling

A better understanding of the mode of action of postharvest biocontrol agents on fruit surfaces is critical for the advancement of successful implementation of postharvest biocontrol products. This is due to the increasing importance of biological control of postharvest diseases over chemical and other control methods. However, most of the mechanisms involved in biological control remain unknown and need to be explored. Yarrowia lipolytica significantly inhibited blue mold decay of apples caused by Penicillium expansum. The findings also demonstrated that Y. lipolytica stimulated the activities of polyphenoloxidase, peroxidase, chitinase, l-phenylalanine ammonia lyase involved in enhancing defense responses in apple fruit tissue. Proteomic and transcriptomic analysis revealed a total of 35 proteins identified as up- and down-regulated in response to the Y. lipolytica inducement. These proteins were related to defense, biotic stimulus, and stress responses, such as pathogenesis-related proteins and dehydrin. The analysis of the transcriptome results proved that the induced resistance was mediated by a crosstalk between salicylic acid (SA) and ethylene/jasmonate (ET/JA) pathways. Y. lipolytica treatment activated the expression of isochorismate synthase gene in the SA pathway, which up-regulates the expression of PR4 in apple. The expression of 1-aminocyclopropane-1-carboxylate oxidase gene and ET-responsive transcription factors 2 and 4, which are involved in the ET pathway, were also activated. In addition, cytochrome oxidase I, which plays an important role in JA signaling for resistance acquisition, was also activated. However, not all of the genes had a positive effect on the SA and ET/JA signal pathways. As transcriptional repressors in JA signaling, TIFY3B and TIFY11B were triggered by the yeast, but the gene expression levels were relatively low. Taken together, Y. lipolytica induced the SA and ET/JA signal mediating the defense pathways by stimulating defense response genes, such as peroxidase, thaumatin-like protein, and chitinase 4-like, which are involved in defense response in apple. [Formula: see text] Copyright © 2017 The Author(s) This is an open access article distributed under the CC BY-NC-ND 4.0 International license .

Infection-induced rapid cell death in plants: a means of efficient pathogen defense

1995 ◽  
Vol 73 (S1) ◽  
pp. 426-434 ◽  
Author(s):  
Elmon Schmelzer ◽  
Beatrix Naton ◽  
Sibylle Freytag ◽  
Ila Rouhara ◽  
Bernhard Küster ◽  
...  
Keyword(s):  
Cell Death ◽  
Defense Response ◽  
Pathogenic Bacteria ◽  
Cultured Cells ◽  
Defense Responses ◽  
Hypersensitive Reaction ◽  
Cellular Level ◽  
Comprehensive Description ◽  
Hypersensitive Cell Death ◽  
Transient Activation

The hypersensitive reaction represents one of the major means by which plants actively defend themselves against infection by pathogenic bacteria, fungi, viruses, and nematodes. This complex defense reaction, often associated with the synthesis of phytoalexins (antimicrobial secondary metabolites), involves at the cellular level highly dynamic cytoplasmic rearrangements, rapid metabolic changes, and finally cell death. It also correlates with the rapid and transient activation of various defense-related genes in a region of tissue surrounding infection sites and later, with the systemic increase in expression of a number of other genes. Examination of the reactions of individual living cells of potato leaves infected with Phytophthora infestans enabled the comprehensive description of the dynamic aspects of all stages of the defense response. Cytochemical investigations, employing cultured cells of parsley infected with P. infestans as a versatile model system, have contributed to a better understanding of cytoplasmic and metabolic processes occurring during the defense response, and suggest that hypersensitive cell death requires the preceding activation of respiration and specific metabolic pathways. Key words: defense responses, defense-related genes, hypersensitive reaction, programmed cell death.

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