Статті в журналах: "Hypersensitive disease resistance"

1

Park, Jeong-Mee. "The Hypersensitive Response. A Cell Death during Disease Resistance." Plant Pathology Journal 21, no. 2 (January 1, 2005): 99–101. http://dx.doi.org/10.5423/ppj.2005.21.2.099.

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2

Tenhaken, R., A. Levine, L. F. Brisson, R. A. Dixon, and C. Lamb. "Function of the oxidative burst in hypersensitive disease resistance." Proceedings of the National Academy of Sciences 92, no. 10 (May 9, 1995): 4158–63. http://dx.doi.org/10.1073/pnas.92.10.4158.

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3

Yu, Gong-Xin, Ed Braun, and Roger P. Wise. "Rds and Rih Mediate Hypersensitive Cell Death Independent of Gene-for-Gene Resistance to the Oat Crown Rust Pathogen Puccinia coronata f. sp. avenae." Molecular Plant-Microbe Interactions® 14, no. 12 (December 2001): 1376–83. http://dx.doi.org/10.1094/mpmi.2001.14.12.1376.

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The Pca crown rust resistance cluster in the diploid Avena genus confers gene-for-gene specificity to numerous isolates of Puccinia coronata f. sp. avenae. Recombination breakpoint analysis indicates that specificities conferred by the Pca cluster are controlled by at least five distinct genes, designated Pc81, Pc82, Pc83, Pc84, and Pc85. Avena plants with the appropriate genotype frequently respond to P. coronata by undergoing hypersensitive cell death at the sites of fungal infection. Autofluorescence of host cells in response to P. coronata occurs in plants that develop visible necrotic lesions but not in plants that lack this phenotype. Two newly described, non-Pc loci were shown to control hypersensitive cell death. Rds (resistance-dependent suppressor of cell death) suppresses the hypersensitive response (HR), but not the resistance, mediated by the Pc82 resistance gene. In contrast, Rih (resistance-independent hypersensitive cell death) confers HR in both resistant and susceptible plants. Linkage analysis indicates that Rds is unlinked to the Pca cluster, whereas Rih is tightly linked to it. These results indicate that multiple synchronous pathways affect the development of hypersensitive cell death and that HR is not essential for resistance to crown rust. Further characterization of these genes will clarify the relationship between plant disease resistance and localized hypersensitive cell death.

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4

Fontoura, Darci Da, Antonio Carlos Torres Costa, José Renato Stangarlin, and Claudio Yuji Tsutsumi. "Disease resistance induction in second-season corn using acibenzolar-S-methyl and phosphorylated mannanoligosaccharide." Semina: Ciências Agrárias 36, no. 6 (December 9, 2015): 3657. http://dx.doi.org/10.5433/1679-0359.2015v36n6p3657.

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Resistance induction is an alternative method to reduce pesticide use in plant disease control. We conducted experiments with four corn hybrids over two consecutive years (2011 and 2012) in order to test resistance in second-season corn treated with acibenzolar-S-methyl (ASM) or phosphorylated mannanoligosaccharide (MOS). In addition, the plants were subjected to a fungicide (azoxystrobin + cyproconazole) or a control treatment using water only. Distinct pathogens were found in the harvests from both years, but the MOS treatment resulted in hypersensitive response during both years. None of the products applied affected plant height, ear insertion height, or damaged kernel percentage. MOS resulted in higher hypersensitive response intensity, without reducing productivity, compared to the water treatment. The application of ASM did not induce a hypersensitive response.

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5

De Stefano, Matteo, Alberto Ferrarini, and Massimo Delledonne. "Nitric oxide functions in the plant hypersensitive disease resistance response." BMC Plant Biology 5, Suppl 1 (2005): S10. http://dx.doi.org/10.1186/1471-2229-5-s1-s10.

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6

Levine, Alex, Roger I. Pennell, Maria E. Alvarez, Robert Palmer, and Chris Lamb. "Calcium-mediated apoptosis in a plant hypersensitive disease resistance response." Current Biology 6, no. 4 (April 1996): 427–37. http://dx.doi.org/10.1016/s0960-9822(02)00510-9.

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7

VALE, FRANCISCO XAVIER RIBEIRO DO, J. E. PARLEVLIET, and LAÉRCIO ZAMBOLIM. "Concepts in plant disease resistance." Fitopatologia Brasileira 26, no. 3 (September 2001): 577–89. http://dx.doi.org/10.1590/s0100-41582001000300001.

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Resistance to nearly all pathogens occurs abundantly in our crops. Much of the resistance exploited by breeders is of the major gene type. Polygenic resistance, although used much less, is even more abundantly available. Many types of resistance are highly elusive, the pathogen apparently adapting very easily them. Other types of resistance, the so-called durable resistance, remain effective much longer. The elusive resistance is invariably of the monogenic type and usually of the hypersensitive type directed against specialised pathogens. Race-specificity is not the cause of elusive resistance but the consequence of it. Understanding acquired resistance may open interesting approaches to control pathogens. This is even truer for molecular techniques, which already represent an enourmously wide range of possibilities. Resistance obtained through transformation is often of the quantitative type and may be durable in most cases.

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8

Khan, M. A., and R. G. Saini. "Non-hypersensitive leaf rust resistance of bread wheat cultivar PBW65 conditioned by genes different fromLr34." Czech Journal of Genetics and Plant Breeding 45, No. 1 (February 11, 2009): 26–30. http://dx.doi.org/10.17221/51/2008-cjgpb.

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: The bread wheat (Triticum aestivum L.) cultivar PBW65 has shown hight levels of resistance to the most frequent and highly virulent Indian race 77-5 of leaf rust (Puccinia triticina). The infection type and disease severity indicated a non-hypersensitive type of resistance against the race 77-5 in PBW65. The cultivar PBW65 was crossed with the leaf rust susceptible cultivar WL711 to determine the mode of inheritance of the resistance. The segregation for resistant and susceptible plants in the F<sub>2</sub> and F<sub>3</sub> generations revealed, that two genes, each showing additive effects, were likely to confer resistance to leaf rust in PBW65. Intercrossing of PBW65 with Cook (Lr34), RL6058 (Lr34) and HD2009, possessing a similar resistance level like PBW65, revealed that the genes for leaf rust resistance in PBW65 were non-allelic to Cook (Lr34), RL6058 (Lr34) as well as to the gene(s) in HD2009. It is concluded that the cultivar PBW65 is a novel source of non-hypersensitive leaf rust resistance.

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9

Gilroy, Eleanor M., Ingo Hein, Renier Van Der Hoorn, Petra C. Boevink, Eduard Venter, Hazel McLellan, Florian Kaffarnik, et al. "Involvement of cathepsin B in the plant disease resistance hypersensitive response." Plant Journal 52, no. 1 (July 26, 2007): 1–13. http://dx.doi.org/10.1111/j.1365-313x.2007.03226.x.

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10

Cooper, Bret, Kimberly B. Campbell, Hunter S. Beard, Wesley M. Garrett, and Marcio E. Ferreira. "The Proteomics of Resistance to Halo Blight in Common Bean." Molecular Plant-Microbe Interactions® 33, no. 9 (September 2020): 1161–75. http://dx.doi.org/10.1094/mpmi-05-20-0112-r.

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Halo blight disease of beans is caused by a gram-negative bacterium, Pseudomonas syringae pv. phaseolicola. The disease is prevalent in South America and Africa and causes crop loss for indigent people who rely on beans as a primary source of daily nutrition. In susceptible beans, P. syringae pv. phaseolicola causes water-soaking at the site of infection and produces phaseolotoxin, an inhibitor of bean arginine biosynthesis. In resistant beans, P. syringae pv. phaseolicola triggers a hypersensitive response that limits the spread of infection. Here, we used high-throughput mass spectrometry to interrogate the responses to two different P. syringae pv. phaseolicola isolates on a single line of common bean, Phaseolus vulgaris PI G19833, with a reference genome sequence. We obtained quantitative information for 4,135 bean proteins. A subset of 160 proteins with similar accumulation changes during both susceptible and resistant reactions included salicylic acid responders EDS1 and NDR1, ethylene and jasmonic acid biosynthesis enzymes, and proteins enabling vesicle secretion. These proteins revealed the activation of a basal defense involving hormonal responses and the mobilization of extracellular proteins. A subset of 29 proteins specific to hypersensitive immunity included SOBIR1, a G-type lectin receptor–like kinase, and enzymes needed for glucoside and phytoalexin production. Virus-induced gene silencing revealed that the G-type lectin receptor–like kinase suppresses bacterial infection. Together, the results define the proteomics of disease resistance to P. syringae pv. phaseolicola in beans and support a model whereby the induction of hypersensitive immunity reinstates defenses targeted by P. syringae pv. phaseolicola.

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11

Hofius, D., D. Munch, S. Bressendorff, J. Mundy, and M. Petersen. "Role of autophagy in disease resistance and hypersensitive response-associated cell death." Cell Death & Differentiation 18, no. 8 (April 29, 2011): 1257–62. http://dx.doi.org/10.1038/cdd.2011.43.

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12

Levine, Alex, Raimund Tenhaken, Richard Dixon, and Chris Lamb. "H2O2 from the oxidative burst orchestrates the plant hypersensitive disease resistance response." Cell 79, no. 4 (November 1994): 583–93. http://dx.doi.org/10.1016/0092-8674(94)90544-4.

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13

Sharma, Sadikshya, and Krishna Bhattarai. "Progress in Developing Bacterial Spot Resistance in Tomato." Agronomy 9, no. 1 (January 9, 2019): 26. http://dx.doi.org/10.3390/agronomy9010026.

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Bacterial spot (BS), caused by four species of Xanthomonas: X. euvesicatoria, X. vesicatoria, X. perforans and X. gardneri in tomato (Solanum lycopersicum L.) results in severe loss in yield and quality by defoliation and the appearance of lesions on fruits, respectively. The combined industry standard for BS control (foliar applications Actigard® rotated with copper plus mancozeb) does not offer sufficient protection, especially when weather conditions favor disease spread. Development of tomato cultivars with BS resistance is thus an important measure to minimize losses. Hypersensitive and non-hypersensitive resistance has been identified in different wild accessions and cultivated tomato relatives and has been transferred to cultivated tomato. However, complete resistance is yet to be obtained. With the advent of next generation sequencing and precise genome editing tools, the genetic regions that confer resistance to bacterial spot can be targeted and enriched through gene pyramiding in a new commercial cultivar which may confer higher degree of horizontal resistance to multiple strains of Xanthomonas causing bacterial spot in tomato.

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14

Singh, R. P., T. S. Payne, P. Figueroa, and S. Valenzuela. "Comparison of the effect of leaf rust on the grain yield of resistant, partially resistant, and susceptible spring wheat cultivars." American Journal of Alternative Agriculture 6, no. 3 (September 1991): 115–21. http://dx.doi.org/10.1017/s0889189300004069.

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AbstractThree hypersensitive resistant, six partially resistant (slow rusting), and one susceptible spring bread wheat (Triticum aestivum L.) cultivars were evaluated for grain yield, test weight, and kernel weight under artificially created epiphytotics of leaf rust disease (caused by Puccinia recondita f. sp. tritici) with and without fungicide protection for three years. Rusted plot yields were 4 percent lower compared to fungicide-protected plot yields for cultivars with hypersensitive resistance. In rusted plots, grain yield and kernel weight averaged 8 percent less for cultivars with partial resistance but varied from 2 to 20 percent less depending on cultivar. The susceptible check cultivar, Yecora 70, averaged 27 percent lower grain yield, 22 percent lower kernel weight, and 6 percent lower test weight in rusted plots. Slight reduction in test weight was also observed for each cultivar. Losses in grain yield could, therefore, be reduced to levels similar to those of hypersensitive resistant cultivars by the use of partial resistance. We discuss the sustainability of partial genetic resistance to leaf rust. Since partial resistance is expected to be durable, and since rust levels and effects on yield in farmers' fields are likely to be less than in this experimental plot study, partial resistance should give long-lasting resistance at a negligible cost in yield that is insufficient to justify the use of fungicides.

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15

Ger, Mang-jye, Cheng-hsien Chen, Shaw-yhi Hwang, Hsiang-en Huang, Appa Rao Podile, Badri Venkata Dayakar, and Teng-yung Feng. "Constitutive Expression of hrap Gene in Transgenic Tobacco Plant Enhances Resistance Against Virulent Bacterial Pathogens by Induction of a Hypersensitive Response." Molecular Plant-Microbe Interactions® 15, no. 8 (August 2002): 764–73. http://dx.doi.org/10.1094/mpmi.2002.15.8.764.

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Hypersensitive response-assisting protein (HRAP) has been previously reported as an amphipathic plant protein isolated from sweet pepper that intensifies the harpinPss-mediated hypersensitive response (HR). The hrap gene has no appreciable similarity to any other known sequences, and its activity can be rapidly induced by incompatible pathogen infection. To assess the function of the hrap gene in plant disease resistance, the CaMV 35S promoter was used to express sweet pepper hrap in transgenic tobacco. Compared with wild-type tobacco, transgenic tobacco plants exhibit more sensitivity to harpinPss and show resistance to virulent pathogens (Pseudomonas syringae pv. tabaci and Erwinia carotovora subsp. carotovora). This disease resistance of transgenic tobacco does not originate from a constitutive HR, because endogenous level of salicylic acid and hsr203J mRNA showed similarities in transgenic and wild-type tobacco under noninfected conditions. However, following a virulent pathogen infection in hrap transgenic tobacco, hsr203J was rapidly induced and a micro-HR necrosis was visualized by trypan blue staining in the infiltration area. Consequently, we suggest that the disease resistance of transgenic plants may result from the induction of a HR by a virulent pathogen infection.

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16

Calderón-González, Álvaro, Javier Matías, Verónica Cruz, Leire Molinero-Ruiz, and Sara Fondevilla. "Identification and Characterization of Sources of Resistance to Peronospora variabilis in Quinoa." Agronomy 13, no. 2 (January 17, 2023): 284. http://dx.doi.org/10.3390/agronomy13020284.

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Downy mildew, caused by Peronospora variabilis, is the most important quinoa disease worldwide. However, little is known about the resistance mechanisms acting against this disease. The study goals were to identify quinoa accessions showing resistance to P. variabilis under Spanish field conditions and to characterize the resistance mechanism involved. Towards these objectives, a total amount of 229 accessions of Chenopodium quinoa and one accession of each of the species Chenopodiun berlandieri subs. nutillae, Chenopodium ugandae, and Chenopodium opulifolium were screened for resistance to P. variabilis under field conditions in Córdoba, Spain, during two seasons. The response to P. variabilis in the accessions showed a continuous distribution ranging from complete resistance to high susceptibility. Fifteen resistant and one susceptible accessions were selected for further histological studies. Histological results showed that resistance to downy mildew in quinoa acts mainly at the stage of colony establishment. In resistant accessions, no colonies were formed or success in colony establishment was significantly reduced compared with the susceptible control. Hypersensitive response was associated with colony abortion in a number of the resistant accessions. This work is the first proof of hypersensitive reaction occurrence in quinoa as a response to P. variabilis.

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17

Yu, I. c., J. Parker, and A. F. Bent. "Gene-for-gene disease resistance without the hypersensitive response in Arabidopsis dnd1 mutant." Proceedings of the National Academy of Sciences 95, no. 13 (June 23, 1998): 7819–24. http://dx.doi.org/10.1073/pnas.95.13.7819.

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18

Loake, Gary John, Byung Wook Yun, Angela Feechan, Jacqueline Pallas, and Eunjung Kwon. "O05. S-nitrosothiols regulate hypersensitive cell death during the plant disease resistance response." Nitric Oxide 14, no. 4 (June 2006): 2. http://dx.doi.org/10.1016/j.niox.2006.04.009.

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19

Eldan, Or, Arie Ofir, Neta Luria, Chen Klap, Oded Lachman, Elena Bakelman, Eduard Belausov, Elisheva Smith, and Aviv Dombrovsky. "Pepper Plants Harboring L Resistance Alleles Showed Tolerance toward Manifestations of Tomato Brown Rugose Fruit Virus Disease." Plants 11, no. 18 (September 12, 2022): 2378. http://dx.doi.org/10.3390/plants11182378.

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The tobamovirus tomato brown rugose fruit virus (ToBRFV) infects tomato plants harboring the Tm-22 resistance allele, which corresponds with tobamoviruses’ avirulence (Avr) gene encoding the movement protein to activate a resistance-associated hypersensitive response (HR). ToBRFV has caused severe damage to tomato crops worldwide. Unlike tomato plants, pepper plants harboring the L resistance alleles, which correspond with the tobamovirus Avr gene encoding the coat protein, have shown HR manifestations upon ToBRFV infection. We have found that ToBRFV inoculation of a wide range of undefined pepper plant varieties could cause a “hypersensitive-like cell death” response, which was associated with ToBRFV transient systemic infection dissociated from disease symptom manifestations on fruits. Susceptibility of pepper plants harboring L1, L3, or L4 resistance alleles to ToBRFV infection following HRs was similarly transient and dissociated from disease symptom manifestations on fruits. Interestingly, ToBRFV stable infection of a pepper cultivar not harboring the L gene was also not associated with disease symptoms on fruits, although ToBRFV was localized in the seed epidermis, parenchyma, and endothelium, which borders the endosperm, indicating that a stable infection of maternal origin of these tissues occurred. Pepper plants with systemic ToBRFV infection could constitute an inoculum source for adjacently grown tomato plants.

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20

Choi, Hyong Woo, Young Jin Kim, and Byung Kook Hwang. "The Hypersensitive Induced Reaction and Leucine-Rich Repeat Proteins Regulate Plant Cell Death Associated with Disease and Plant Immunity." Molecular Plant-Microbe Interactions® 24, no. 1 (January 2011): 68–78. http://dx.doi.org/10.1094/mpmi-02-10-0030.

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Pathogen-induced programmed cell death (PCD) is intimately linked with disease resistance and susceptibility. However, the molecular components regulating PCD, including hypersensitive and susceptible cell death, are largely unknown in plants. In this study, we show that pathogen-induced Capsicum annuum hypersensitive induced reaction 1 (CaHIR1) and leucine-rich repeat 1 (CaLRR1) function as distinct plant PCD regulators in pepper plants during Xanthomonas campestris pv. vesicatoria infection. Confocal microscopy and protein gel blot analyses revealed that CaLRR1 and CaHIR1 localize to the extracellular matrix and plasma membrane (PM), respectively. Bimolecular fluorescent complementation and coimmunoprecipitation assays showed that the extracellular CaLRR1 specifically binds to the PM-located CaHIR1 in pepper leaves. Overexpression of CaHIR1 triggered pathogen-independent cell death in pepper and Nicotiana benthamiana plants but not in yeast cells. Virus-induced gene silencing (VIGS) of CaLRR1 and CaHIR1 distinctly strengthened and compromised hypersensitive and susceptible cell death in pepper plants, respectively. Endogenous salicylic acid levels and pathogenesis-related gene transcripts were elevated in CaHIR1-silenced plants. VIGS of NbLRR1 and NbHIR1, the N. benthamiana orthologs of CaLRR1 and CaHIR1, regulated Bax- and avrPto-/Pto-induced PCD. Taken together, these results suggest that leucine-rich repeat and hypersensitive induced reaction proteins may act as cell-death regulators associated with plant immunity and disease.

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21

Yu, Guangchao, Xiangyu Wang, Qiumin Chen, Na Cui, Yang Yu, and Haiyan Fan. "Cucumber Mildew Resistance Locus O Interacts with Calmodulin and Regulates Plant Cell Death Associated with Plant Immunity." International Journal of Molecular Sciences 20, no. 12 (June 19, 2019): 2995. http://dx.doi.org/10.3390/ijms20122995.

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Pathogen-induced cell death is closely related to plant disease susceptibility and resistance. The cucumber (Cucumis sativus L.) mildew resistance locus O (CsMLO1) and calmodulin (CsCaM3) genes, as molecular components, are linked to nonhost resistance and hypersensitive cell death. In this study, we demonstrate that CsMLO1 interacts with CsCaM3 via yeast two-hybrid, firefly luciferase (LUC) complementation and bimolecular fluorescence complementation (BiFC) experiments. A subcellular localization analysis of green fluorescent protein (GFP) fusion reveals that CsCaM3 is transferred from the cytoplasm to the plasma membrane in Nicotiana benthamiana, and CsCaM3 green fluorescence is significantly attenuated via the coexpression of CsMLO1 and CsCaM3. CsMLO1 negatively regulates CsCaM3 expression in transiently transformed cucumbers, and hypersensitive cell death is disrupted by CsCaM3 and/or CsMLO1 expression under Corynespora cassiicola infection. Additionally, CsMLO1 silencing significantly enhances the expression of reactive oxygen species (ROS)-related genes (CsPO1, CsRbohD, and CsRbohF), defense marker genes (CsPR1 and CsPR3) and callose deposition-related gene (CsGSL) in infected cucumbers. These results suggest that the interaction of CsMLO1 with CsCaM3 may act as a cell death regulator associated with plant immunity and disease.

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22

Delledonne, Massimo, Irene Murgia, Davide Ederle, Pier Filippo Sbicego, Andrea Biondani, Annalisa Polverari, and Chris Lamb. "Reactive oxygen intermediates modulate nitric oxide signaling in the plant hypersensitive disease-resistance response." Plant Physiology and Biochemistry 40, no. 6-8 (June 2002): 605–10. http://dx.doi.org/10.1016/s0981-9428(02)01397-9.

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23

Künstler, András, Renáta Bacsó, Gábor Gullner, Yaser Mohamed Hafez, and Lóránt Király. "Staying alive – is cell death dispensable for plant disease resistance during the hypersensitive response?" Physiological and Molecular Plant Pathology 93 (January 2016): 75–84. http://dx.doi.org/10.1016/j.pmpp.2016.01.003.

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24

Zaninotto, Federica, Sylvain La Camera, Annalisa Polverari, and Massimo Delledonne. "Cross Talk between Reactive Nitrogen and Oxygen Species during the Hypersensitive Disease Resistance Response." Plant Physiology 141, no. 2 (June 2006): 379–83. http://dx.doi.org/10.1104/pp.106.078857.

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25

Delledonne, M., and M. Romero-Puertas. "S-nitrosylation inhibits peroxiredoxin II E functions during the plant hypersensitive disease resistance response." Comparative Biochemistry and Physiology Part A: Molecular & Integrative Physiology 146, no. 4 (April 2007): S255—S256. http://dx.doi.org/10.1016/j.cbpa.2007.01.642.

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26

Yu, I.-ching, Kevin A. Fengler, Steven J. Clough, and Andrew F. Bent. "Identification of Arabidopsis Mutants Exhibiting an Altered Hypersensitive Response in Gene-for-Gene Disease Resistance." Molecular Plant-Microbe Interactions® 13, no. 3 (March 2000): 277–86. http://dx.doi.org/10.1094/mpmi.2000.13.3.277.

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A mutational study was carried out to isolate Arabidopsis thaliana plants that exhibit full or partial disruption of the RPS2-mediated hypersensitive response (HR) to Pseudomonas syringae that express avrRpt2. Five classes of mutants were identified including mutations at RPS2, dnd mutations causing a “defense, no death” loss-of-HR phenotype, a lesion-mimic mutant that also exhibited an HR¯phenotype, and a number of intermediate or partial-loss-of-HR mutants. Surprisingly, many of these mutants displayed elevated resistance to virulent P. syringae and, in some cases, to Peronospora parasitica. Constitutively elevated levels of pathogenesis-related (PR) gene expression and salicylic acid were also observed. In the lesion-mimic mutant, appearance of elevated resistance was temporally correlated with appearance of lesions. For one of the intermediate lines, resistance was shown to be dependent on elevated levels of salicylic acid. A new locus was identified and named IHR1, after the mutant phenotype of “intermediate HR.” Genetic analysis of the intermediate-HR plant lines was difficult due to uncertainties in distinguishing the partial/intermediate mutant phenotypes from wild type. Despite this difficulty, the intermediate-HR mutants remain of interest because they reveal potential new defense-related loci and because many of these lines exhibit partially elevated disease resistance without dwarfing or other apparent growth defects.

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27

Sánchez, Gerardo, Nadia Gerhardt, Florencia Siciliano, Adrián Vojnov, Isabelle Malcuit, and María Rosa Marano. "Salicylic Acid Is Involved in the Nb-Mediated Defense Responses to Potato virus X in Solanum tuberosum." Molecular Plant-Microbe Interactions® 23, no. 4 (April 2010): 394–405. http://dx.doi.org/10.1094/mpmi-23-4-0394.

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To evaluate the role of salicylic acid (SA) in Nb-mediated hypersensitive resistance to Potato virus X (PVX) avirulent strain ROTH1 in Solanum tuberosum, we have constructed SA-deficient transgenic potato plant lines by overexpressing the bacterial enzyme salicylate hydroxylase (NahG), which degrades SA. Evaluation of these transgenic lines revealed hydrogen peroxide accumulation and spontaneous lesion formation in an age- and light-dependent manner. In concordance, NahG potato plants were more sensitive to treatment with methyl viologen, a reactive oxygen species–generating compound. In addition, when challenged with PVX ROTH1, NahG transgenic lines showed a decreased disease-resistance response to infection and were unable to induce systemic acquired resistance. However, the avirulent viral effector, the PVX 25-kDa protein, does induce expression of the pathogenesis-related gene PR-1a in NahG potato plants. Taken together, our data indicate that SA is involved in local and systemic defense responses mediated by the Nb gene in Solanum tuberosum. This is the first report to show that basal levels of SA correlate with hypersensitive resistance to PVX.

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28

Sbaihat, Layth, Keiko Takeyama, Takeharu Koga, Daigo Takemoto, and Kazuhito Kawakita. "Induced Resistance inSolanum lycopersicumby Algal Elicitor Extracted fromSargassum fusiforme." Scientific World Journal 2015 (2015): 1–9. http://dx.doi.org/10.1155/2015/870520.

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Tomato (Solanum lycopersicum) production relies heavily on the use of chemical pesticides, which is undesired by health- and environment-concerned consumers. Environment-friendly methods of controlling tomato diseases include agroecological practices, organic fungicides, and biological control. Plants’ resistance against pathogens is induced by applying agents called elicitors to the plants and would lead to disease prevention or reduced severity. We investigated the ability of a novel elicitor extracted from the brown sea algae (Sargassum fusiforme) to elicit induced resistance in tomato. The studied elicitor induced hypersensitive cell death andO2-production in tomato tissues. It significantly reduced severities of late blight, grey mold, and powdery mildew of tomato. Taken together, our novel elicitor has not shown any direct antifungal activity against the studied pathogens, concluding that it is an elicitor of induced resistance.

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29

Jiang, Xiuming, Yang Li, Ran Li, Yijie Gao, Zengbing Liu, Huanhuan Yang, Jingfu Li, Jingbin Jiang, Tingting Zhao, and Xiangyang Xu. "Transcriptome Analysis of the Cf-13-Mediated Hypersensitive Response of Tomato to Cladosporium fulvum Infection." International Journal of Molecular Sciences 23, no. 9 (April 27, 2022): 4844. http://dx.doi.org/10.3390/ijms23094844.

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Tomato leaf mold disease caused by Cladosporium fulvum (C. fulvum) is one of the most common diseases affecting greenhouse tomato production. Cf proteins can recognize corresponding AVR proteins produced by C. fulvum, and Cf genes are associated with leaf mold resistance. Given that there are many physiological races of C. fulvum and that these races rapidly mutate, resistance to common Cf genes (such as Cf-2, Cf-4, Cf-5, and Cf-9) has decreased. In the field, Ont7813 plants (carrying the Cf-13 gene) show effective resistance to C. fulvum; thus, these plants could be used as new, disease-resistant materials. To explore the mechanism of the Cf-13-mediated resistance response, transcriptome sequencing was performed on three replicates each of Ont7813 (Cf-13) and Moneymaker (MM; carrying the Cf-0 gene) at 0, 9, and 15 days after inoculation (dai) for a total of 18 samples. In total, 943 genes were differentially expressed, specifically in the Ont7813 response process as compared to the Moneymaker response process. Gene ontology (GO) classification of these 943 differentially expressed genes (DEGs) showed that GO terms, including “hydrogen peroxide metabolic process (GO_Process)”, “secondary active transmembrane transporter activity (GO_Function)”, and “mismatch repair complex (GO_Component)”, which were the same as 11 other GO terms, were significantly enriched. An analysis of the Kyoto Encyclopedia of Genes and Genomes (KEGG) revealed that many key regulatory genes of the Cf-13-mediated resistance response processes were involved in the “plant hormone signal transduction” pathway, the “plant–pathogen interaction” pathway, and the “MAPK signaling pathway–plant” pathway. Moreover, during C. fulvum infection, jasmonic acid (JA) and salicylic acid (SA) contents significantly increased in Ont7813 at the early stage. These results lay a vital foundation for further understanding the molecular mechanism of the Cf-13 gene in response to C. fulvum infection.

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30

Wroth, J. M. "Possible role for wild genotypes of Pisum spp. to enhance ascochyta blight resistance in pea." Australian Journal of Experimental Agriculture 38, no. 5 (1998): 469. http://dx.doi.org/10.1071/ea98024.

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Summary. There are no cultivars with effective field resistance to ascochyta blight currently available in Australia but a number of wild genotypes of Pisum have been identified as possible sources of resistance and these were evaluated in crosses with a commercial cultivar. Pisum fulvum JI 1006, used as the pollen parent, was crossed with P. sativum cv. Wirrega using wild type P. sativum JI 252 as a bridging cross. JI 1006 and JI 252 both respond to Mycosphaerella pinodes infection by inducing a rapid hypersensitive response. All F2 seedlings (17–20-day-old) from the cross Wirrega × (JI 252 × JI 1006) were screened for their responses to M. pinodes infection in a controlled environment and plants with the highest levels of resistance were then screened as F3 progeny families in the field to determine their responses to natural M. pinodes infection. Nine percent of these families were significantly more resistant for both leaf and stem disease compared with Wirrega and among them were 9 lines which flowered at the same time or earlier than Wirrega. However, even the most resistant line had 30% of the foliage destroyed by disease, indicating disease control was insufficient. A second resistance mechanism which impeded M. pinodes hyphal penetration in leaves (P. sativum SA 1160) was combined with the hypersensitive response in the cross SA 1160 × (JI 252 × JI 1006). The level of resistance to disease was now significantly higher than any plant in the original F3 population, despite the wild-type growth habit of these plants. It is suggested that breeding programs should focus first on maximising field resistance through isolation of some optimal combinations of resistance mechanisms in wild genotypes before turning to improving the agronomic performance through backcrossing to advanced breeding lines.

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31

Liu, Fang, Yunjian Xu, Lingyan Zhou, Asif Ali, Haiyang Jiang, Suwen Zhu, and Xiaoyu Li. "DNA Repair Gene ZmRAD51A Improves Rice and Arabidopsis Resistance to Disease." International Journal of Molecular Sciences 20, no. 4 (February 13, 2019): 807. http://dx.doi.org/10.3390/ijms20040807.

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RAD51 (DNA repair gene) family genes play ubiquitous roles in immune response among species from plants to mammals. In this study, we cloned the ZmRAD51A gene (a member of RAD51) in maize and generated ZmRAD51A overexpression (ZmRAD51A-OE) in rice, tobacco, and Arabidopsis. The expression level of ZmRAD51A was remarkably induced by salicylic acid (SA) application in maize, and the transient overexpression of ZmRAD51A in tobacco induced a hypersensitive response. The disease resistance was significantly enhanced in ZmRAD51A- OE (overexpressing) plants, triggering an increased expression of defense-related genes. High-performance liquid chromatography (HPLC) analysis showed that, compared to control lines, ZmRAD51A-OE in rice plants resulted in higher SA levels, and conferred rice plants resistance to Magnaporthe oryzae. Moreover, the ZmRAD51A-OE Arabidopsis plants displayed increased resistance to Pseudomonas syringae pv. tomato DC3000 when compared to wild types. Together, our results provide the evidence that, for the first time, the maize DNA repair gene ZmRAD51A plays an important role in in disease resistance.

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32

Gassmann, Walter. "Natural Variation in the Arabidopsis Response to the Avirulence Gene hopPsyA Uncouples the Hypersensitive Response from Disease Resistance." Molecular Plant-Microbe Interactions® 18, no. 10 (October 2005): 1054–60. http://dx.doi.org/10.1094/mpmi-18-1054.

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The plant hypersensitive response (HR) is tightly associated with gene-for-gene resistance and has been proposed to function in containing pathogens at the invasion site. This tight association has made it difficult to unequivocally evaluate the importance of HR for plant disease resistance. Here, hopPsyA from Pseudomonas syringae pv. syringae 61 is identified as a new avirulence gene for Arabidopsis that triggers resistance in the absence of macroscopic HR. Resistance to P. syringae pv. tomato DC3000 expressing hopPsyA was EDS1-dependent and NDR1-independent. Intriguingly, several Arabidopsis accessions were resistant to DC3000(hopPsyA) in the absence of HR. This is comparable to the Arabidopsis response to avrRps4, but it is shown that hopPsyA does not signal through RPS4. In a cross between two hopPsyA-resistant accessions that differ in their HR response, the HR segregated as a recessive phenotype regulated by a single locus. This locus, HED1 (HR regulator in EDS1 pathway), is proposed to encode a protein whose activity can cause suppression of the EDS1-dependent HR signaling pathway. HED1-regulated symptomless gene-for-gene resistance responses may explain some cases of Arabidopsis resistance to bacteria that are classified as nonhost resistance.

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33

Keller, Harald, Nicole Pamboukdjian, Michel Ponchet, Alain Poupet, Rene Delon, Jean-Louis Verrier, Dominique Roby, and Pierre Ricci. "Pathogen-Induced Elicitin Production in Transgenic Tobacco Generates a Hypersensitive Response and Nonspecific Disease Resistance." Plant Cell 11, no. 2 (February 1999): 223. http://dx.doi.org/10.2307/3870852.

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34

Keller, Harald, Nicole Pamboukdjian, Michel Ponchet, Alain Poupet, René Delon, Jean-Louis Verrier, Dominique Roby, and Pierre Ricci. "Pathogen-Induced Elicitin Production in Transgenic Tobacco Generates a Hypersensitive Response and Nonspecific Disease Resistance." Plant Cell 11, no. 2 (February 1999): 223–35. http://dx.doi.org/10.1105/tpc.11.2.223.

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35

Baidya, Suraj, Subash C. Bhardwaj, Sundar M. Shrestha, Baidya N. Mahto, and Hira K. Manandhar. "Characterization of Yellow Rust (Puccinia striiformis) Resistance and Genetic Diversity in Nepalese Wheat Genotypes." Journal of the Plant Protection Society 5 (December 31, 2018): 175–93. http://dx.doi.org/10.3126/jpps.v5i0.47129.

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Wheat (Triticum aestivum L.) is third important crop in Nepal after rice and maize. Yellow rust caused by Puccinia striiformis Westend. is a major disease of hills and adjoining foot hills. Both seedling and adult plant stage evaluations were carried out to characterize yellow rust resistance (Yr) genes in 105 Nepalese wheat genotypes at ICAR- Indian Wheat and Barley Research Institute, Regional Station, Shimla India. Eleven pathotypes of P. striiformis were used in seedling evaluation for identifying the resistance gene/s for yellow rust disease. Two most virulent and predominant pathotypes 78S84 and 46S119 were used to screen for adult plant resistance (APR). Four different resistance genes were inferred in tested material viz, YrA, Yr2, Yr9 and Yr27 by the seedling test. The postulated genes were observed either singly or in combination with other gene/s. The resistance genes YrA and Yr2 were detected alone whereas Yr27 was postulated in combination with Yr9. Among them, Yr9 was most dominant gene and was postulated in 48 genotypes either singly or in combination with Yr27. Twenty-one genotypes were found to confer low infection types (ITs) with hypersensitive and non-hypersensitive reaction against all the tested pathotypes. Twenty two of genotypes showed APR to both the pathotypes whereas 43 genotypes showed susceptibility to both pathotypes. In which 16 genotypes had susceptible response both seedling and Adult plant stage against both the pathotypes. Likewise, 53 genotypes had APR to one or other pathotype.

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36

WANI, Shabir Hussain. "Inducing Fungus-Resistance into Plants through Biotechnology." Notulae Scientia Biologicae 2, no. 2 (June 13, 2010): 14–21. http://dx.doi.org/10.15835/nsb224594.

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Plant diseases are caused by a variety of plant pathogens including fungi, and their management requires the use of techniques like transgenic technology, molecular biology, and genetics. There have been attempts to use gene technology as an alternative method to protect plants from microbial diseases, in addition to the development of novel agrochemicals and the conventional breeding of resistant cultivars. Various genes have been introduced into plants, and the enhanced resistance against fungi has been demonstrated. These include: genes that express proteins, peptides, or antimicrobial compounds that are directly toxic to pathogens or that reduce their growth in situ; gene products that directly inhibit pathogen virulence products or enhance plant structural defense genes, that directly or indirectly activate general plant defense responses; and resistance genes involved in the hypersensitive response and in the interactions with virulence factors. The introduction of the tabtoxin acetyltransferase gene, the stilbene synthase gene, the ribosome-inactivation protein gene and the glucose oxidase gene brought enhanced resistance in different plants. Genes encoding hydrolytic enzymes such as chitinase and glucanase, which can deteriorate fungal cell-wall components, are attractive candidates for this approach and are preferentially used for the production of fungal disease-resistant plants. In addition to this, RNA-mediated gene silencing is being tried as a reverse tool for gene targeting in plant diseases caused by fungal pathogens. In this review, different mechanisms of fungal disease resistance through biotechnological approaches are discussed and the recent advances in fungal disease management through transgenic approach are reviewed.

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37

Morel, Jean-Benoit, and Jeffery L. Dangl. "Suppressors of the Arabidopsis lsd5 Cell Death Mutation Identify Genes Involved in Regulating Disease Resistance Responses." Genetics 151, no. 1 (January 1, 1999): 305–19. http://dx.doi.org/10.1093/genetics/151.1.305.

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Abstract Cell death is associated with the development of the plant disease resistance hypersensitive reaction (HR). Arabidopsis lsd mutants that spontaneously exhibit cell death reminiscent of the HR were identified previously. To study further the regulatory context in which cell death acts during disease resistance, one of these mutants, lsd5, was used to isolate new mutations that suppress its cell death phenotype. Using a simple lethal screen, nine lsd5 cell death suppressors, designated phx (for the mythological bird Phoenix that rises from its ashes), were isolated. These mutants were characterized with respect to their response to a bacterial pathogen and oomycete parasite. The strongest suppressors—phx2, 3, 6, and 11-1—showed complex, differential patterns of disease resistance modifications. These suppressors attenuated disease resistance to avirulent isolates of the biotrophic Peronospora parasitica pathogen, but only phx2 and phx3 altered disease resistance to avirulent strains of Pseudomonas syringae pv tomato. Therefore, some of these phx mutants define common regulators of cell death and disease resistance. In addition, phx2 and phx3 exhibited enhanced disease susceptibility to different virulent pathogens, confirming probable links between the disease resistance and susceptibility pathways.

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38

Romero, A. M., and D. F. Ritchie. "Systemic Acquired Resistance Delays Race Shifts to Major Resistance Genes in Bell Pepper." Phytopathology® 94, no. 12 (December 2004): 1376–82. http://dx.doi.org/10.1094/phyto.2004.94.12.1376.

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The lack of durability of host plant disease resistance is a major problem in disease control. Genotype-specific resistance that involves major resistance (R) genes is especially prone to failure. The compatible (i.e., disease) host-pathogen interaction with systemic acquired resistance (SAR) has been studied extensively, but the incompatible (i.e., resistant) interaction less so. Using the pepper-bacterial spot (causal agent, Xanthomonas axonopodis pv. vesicatoria) pathosystem, we examined the effect of SAR in reducing the occurrence of race-change mutants that defeat R genes in laboratory, greenhouse, and field experiments. Pepper plants carrying one or more R genes were sprayed with the plant defense activator acibenzolar-S-methyl (ASM) and challenged with incompatible strains of the pathogen. In the greenhouse, disease lesions first were observed 3 weeks after inoculation. ASM-treated plants carrying a major R gene had significantly fewer lesions caused by both the incompatible (i.e., hypersensitive) and compatible (i.e., disease) responses than occurred on nonsprayed plants. Bacteria isolated from the disease lesions were confirmed to be race-change mutants. In field experiments, there was a delay in the detection of race-change mutants and a reduction in disease severity. Decreased disease severity was associated with a reduction in the number of race-change mutants and the suppression of disease caused by the race-change mutants. This suggests a possible mechanism related to a decrease in the pathogen population size, which subsequently reduces the number of race-change mutants for the selection pressure of R genes. Thus, inducers of SAR are potentially useful for increasing the durability of genotype-specific resistance conferred by major R genes.

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39

Maleck, Klaus, Urs Neuenschwander, Rebecca M. Cade, Robert A. Dietrich, Jeffery L. Dangl, and John A. Ryals. "Isolation and Characterization of Broad-Spectrum Disease-Resistant Arabidopsis Mutants." Genetics 160, no. 4 (April 1, 2002): 1661–71. http://dx.doi.org/10.1093/genetics/160.4.1661.

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Abstract To identify Arabidopsis mutants that constitutively express systemic acquired resistance (SAR), we constructed reporter lines expressing the firefly luciferase gene under the control of the SAR-inducible PR-1 promoter (PR-1/luc). After EMS mutagenesis of a well-characterized transgenic line, we screened 250,000 M2 plants for constitutive expression of the reporter gene in vivo. From a mutant collection containing several hundred putative mutants, we concentrated on 16 mutants lacking spontaneous hypersensitive response (HR) cell death. We mapped 4 of these constitutive immunity (cim) mutants to chromosome arms. Constitutive expression of disease resistance was established by analyzing responses to virulent Peronospora parasitica and Pseudomonas syringae strains, by RNA blot analysis for endogenous marker genes, and by determination of salicylic acid levels in the mutants. The variety of the cim phenotypes allowed us to define distinct steps in both the canonical SAR signaling pathway and a separate pathway for resistance to Erysiphe cichoracearum, active in only a subset of the mutants.

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40

Gu, Yong–Qiang, and Gregory B. Martin. "Molecular mechanisms involved in bacterial speck disease resistance of tomato." Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 353, no. 1374 (September 29, 1998): 1455–61. http://dx.doi.org/10.1098/rstb.1998.0301.

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An important recent advance in the field of plant–microbe interactions has been the cloning of genes that confer resistance to specific viruses, bacteria, fungi or nematodes. Disease resistance ( R ) genes encode proteins with predicted structural motifs consistent with them having roles in signal recognition and transduction. The future challenge is to understand how R gene products specifically perceive defence–eliciting signals from the pathogen and transduce those signals to pathways that lead to the activation of plant defence responses. In tomatoes, the Pto kinase (product of the Pto R gene) confers resistance to strains of the bacterial speck pathogen, Pseudomonas syringae pv. tomato , that carry the corresponding avirulence gene avrPto . Resistance to bacterial speck disease is initiated by a mechanism involving the physical interaction of the Pto kinase and the AvrPto protein. This recognition event initiates signalling events that lead to defence responses including an oxidative burst, the hypersensitive response and expression of pathogenesis–related genes. Pto–interacting (Pti) proteins have been identified that appear to act downstream of the Pto kinase and our current studies are directed at elucidating the roles of these components.

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Russell, Andrew R., Tom Ashfield, and Roger W. Innes. "Pseudomonas syringae Effector AvrPphB Suppresses AvrB-Induced Activation of RPM1 but Not AvrRpm1-Induced Activation." Molecular Plant-Microbe Interactions® 28, no. 6 (June 2015): 727–35. http://dx.doi.org/10.1094/mpmi-08-14-0248-r.

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The Pseudomonas syringae effector AvrB triggers a hypersensitive resistance response in Arabidopsis and soybean plants expressing the disease resistance (R) proteins RPM1 and Rpg1b, respectively. In Arabidopsis, AvrB induces RPM1-interacting protein kinase (RIPK) to phosphorylate a disease regulator known as RIN4, which subsequently activates RPM1-mediated defenses. Here, we show that AvrPphB can suppress activation of RPM1 by AvrB and this suppression is correlated with the cleavage of RIPK by AvrPphB. Significantly, AvrPphB does not suppress activation of RPM1 by AvrRpm1, suggesting that RIPK is not required for AvrRpm1-induced modification of RIN4. This observation indicates that AvrB and AvrRpm1 recognition is mediated by different mechanisms in Arabidopsis, despite their recognition being determined by a single R protein. Moreover, AvrB recognition but not AvrRpm1 recognition is suppressed by AvrPphB in soybean, suggesting that AvrB recognition requires a similar molecular mechanism in soybean and Arabidopsis. In support of this, we found that phosphodeficient mutations in the soybean GmRIN4a and GmRIN4b proteins are sufficient to block Rpg1b-mediated hypersensitive response in transient assays in Nicotiana glutinosa. Taken together, our results indicate that AvrB and AvrPphB target a conserved defense signaling pathway in Arabidopsis and soybean that includes RIPK and RIN4.

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Zhang, Chu, Annie Tang Gutsche, and Allan D. Shapiro. "Feedback Control of the Arabidopsis Hypersensitive Response." Molecular Plant-Microbe Interactions® 17, no. 4 (April 2004): 357–65. http://dx.doi.org/10.1094/mpmi.2004.17.4.357.

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The plant hypersensitive response (HR) to avirulent bacterial pathogens results from programmed cell death of plant cells in the infected region. Ion leakage and changes in signaling components associated with HR progression were measured. These studies compared Arabidopsis mutants affecting feedback loops with wild-type plants, with timepoints taken hourly. In response to Pseudomonas syringae pv. tomato DC3000·avrB, npr1-2 mutant plants showed increased ion leakage relative to wild-type plants. Hydrogen peroxide accumulation was similar to that in wild type, but salicylic acid accumulation was reduced at some timepoints. With DC3000·avrRpt2, similar trends were seen. In response to DC3000·avrB, ndr1-1 mutant plants showed more ion leakage than wild-type or npr1-2 plants. Hydrogen peroxide accumulation was delayed by approximately 1 h and reached half the level seen with wild-type plants. Salicylic acid accumulation was similar to npr1-2 mutant plants. With DC3000·avrRpt2, ndr1-1 mutant plants showed no ion leakage, no hydrogen peroxide accumulation, and minimal salicylic acid accumulation. Results with a ndr1-1 and npr1-2 double mutant were similar to ndr1-1. A model consistent with these data is presented, in which one positive and two negative regulatory circuits control HR progression. Understanding this circuitry will facilitate HR manipulation for enhanced disease resistance.

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Lee, Byung Kook, Beom Seok Kim, Seog Won Chang, and Byung Kook Hwang. "Aggressiveness to Pumpkin Cultivars of Isolates of Phytophthora capsici from Pumpkin and Pepper." Plant Disease 85, no. 5 (May 2001): 497–500. http://dx.doi.org/10.1094/pdis.2001.85.5.497.

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Nine isolates of Phytophthora capsici obtained from pumpkin and pepper in diverse geographic areas, including Korea, France, Italy, and the United States, were evaluated for their ability to cause disease on nine Korean and Japanese pumpkin cultivars under controlled environmental conditions. No hypersensitive type of resistance was observed in any of the pumpkin cultivars inoculated with P. capsici. Disease incidence ranged from low to high, indicating varying levels of partial (quantitative) resistance. In addition, a significant cultivar-isolate interaction was observed, indicating that host specialization was present in some cultivars. Disease severity increased with inoculum density of P. capsici. The Korean cultivar Danmatmaetdol was highly resistant to the P. capsici isolates tested, suggesting that economic levels of resistance exist in pumpkin. The pumpkin isolates from all locations caused more disease than the pepper isolates to all the pumpkin cultivars tested. Soil-drench and stem-wound inoculation methods were more reliable than a foliar-inoculation method for evaluating pumpkin cultivar resistance.

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44

Hemara, Lauren M., Jay Jayaraman, Paul W. Sutherland, Mirco Montefiori, Saadiah Arshed, Abhishek Chatterjee, Ronan Chen, et al. "Effector loss drives adaptation of Pseudomonas syringae pv. actinidiae biovar 3 to Actinidia arguta." PLOS Pathogens 18, no. 5 (May 27, 2022): e1010542. http://dx.doi.org/10.1371/journal.ppat.1010542.

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A pandemic isolate of Pseudomonas syringae pv. actinidiae biovar 3 (Psa3) has devastated kiwifruit orchards growing cultivars of Actinidia chinensis. In contrast, A. arguta (kiwiberry) is not a host of Psa3. Resistance is mediated via effector-triggered immunity, as demonstrated by induction of the hypersensitive response in infected A. arguta leaves, observed by microscopy and quantified by ion-leakage assays. Isolates of Psa3 that cause disease in A. arguta have been isolated and analyzed, revealing a 51 kb deletion in the exchangeable effector locus (EEL). This natural EEL-mutant isolate and strains with synthetic knockouts of the EEL were more virulent in A. arguta plantlets than wild-type Psa3. Screening of a complete library of Psa3 effector knockout strains identified increased growth in planta for knockouts of four effectors–AvrRpm1a, HopF1c, HopZ5a, and the EEL effector HopAW1a –suggesting a resistance response in A. arguta. Hypersensitive response (HR) assays indicate that three of these effectors trigger a host species-specific HR. A Psa3 strain with all four effectors knocked out escaped host recognition, but a cumulative increase in bacterial pathogenicity and virulence was not observed. These avirulence effectors can be used in turn to identify the first cognate resistance genes in Actinidia for breeding durable resistance into future kiwifruit cultivars.

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Barilli, Eleonora, and Diego Rubiales. "Identification and Characterization of Resistance to Rust in Lentil and Its Wild Relatives." Plants 12, no. 3 (January 31, 2023): 626. http://dx.doi.org/10.3390/plants12030626.

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Lentil rust is a major disease worldwide caused by Uromyces viciae-fabae. In this study, we screened a large germplasm collection of cultivated lentils (Lens culinaris ssp. culinaris) and its wild relatives, both in adult plants in the field with a local rust isolate during 2 seasons and in seedlings under controlled conditions with four fungal isolates of worldwide origin. The main results from our study were the following: (1) a significant number of accessions with resistance based on hypersensitive reaction (reduced Infection Type (IT)) were identified in cultivated lentil and in L. ervoides, L. nigricans and L.c. orientalis. The IT scores showed a clear isolate-specific response suggesting race-specificity, so each fungal isolate might be considered a different race. Resistance was identified against all isolates what might be the basis to develop a standard differential set that should be a priority for rust definition and monitoring. (2) Interestingly, although at lower frequency than in L. ervoides and L. nigricans, the hypersensitive response was also observed within cultivated lentil, with accession 1561 (L.c. culinaris) displaying resistance to the four isolates making this accession a valuable ready-to-use resource for lentil resistance breeding. Resistance to all other rust isolates was also available within L.c. culinaris in an isolate-specific manner. Accession 1308 (L. ervoides) showed resistance against all isolates tested, as well as a reduced number of accessions belonging to other wild Lens species. (3) In addition, our screenings allowed the identification of several accessions with partial resistance (reduced Disease Severity (DS) despite high IT). Adult Plant Resistance resulting in reduced severity in adult plants in the field, despite high susceptibility in seedlings, was more frequently identified in L.c. culinaris, but also in L. nigricans and L.c. orientalis.

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Widyasari, Kristin, Mazen Alazem, and Kook-Hyung Kim. "Soybean Resistance to Soybean Mosaic Virus." Plants 9, no. 2 (February 8, 2020): 219. http://dx.doi.org/10.3390/plants9020219.

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Soybean mosaic virus (SMV) occurs in all soybean-growing areas in the world and causes huge losses in soybean yields and seed quality. During early viral infection, molecular interactions between SMV effector proteins and the soybean resistance (R) protein, if present, determine the development of resistance/disease in soybean plants. Depending on the interacting strain and cultivar, R-protein in resistant soybean perceives a specific SMV effector, which triggers either the extreme silent resistance or the typical resistance manifested by hypersensitive responses and induction of salicylic acid and reactive oxygen species. In this review, we consider the major advances that have been made in understanding the soybean–SMV arms race. We also focus on dissecting mechanisms SMV employs to establish infection and how soybean perceives and then responds to SMV attack. In addition, progress on soybean R-genes studies, as well as those addressing independent resistance genes, are also addressed.

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47

Delledonne, M., J. Zeier, A. Marocco, and C. Lamb. "Signal interactions between nitric oxide and reactive oxygen intermediates in the plant hypersensitive disease resistance response." Proceedings of the National Academy of Sciences 98, no. 23 (October 23, 2001): 13454–59. http://dx.doi.org/10.1073/pnas.231178298.

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48

Ariyarathne, H. M., D. P. Coyne, G. Jung, P. W. Skroch, A. K. Vidaver, J. R. Steadman, P. N. Miklas, and M. J. Bassett. "Molecular Mapping of Disease Resistance Genes for Halo Blight, Common Bacterial Blight, and Bean Common Mosaic Virus in a Segregating Population of Common Bean." Journal of the American Society for Horticultural Science 124, no. 6 (November 1999): 654–62. http://dx.doi.org/10.21273/jashs.124.6.654.

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Diseases of beans (Phaseolus vulgaris L.) are primary constraints affecting bean production. Information on tagging and mapping of genes for disease resistance is expected to be useful to breeders. The objectives of this study were to develop a random amplified polymorphic DNA (RAPD) marker linkage map using 78 F9 recombinant inbred (RI) lines derived from a Middle-American common bean cross Great Northern Belneb RR-1 [resistant to common bacterial blight (CBB) and halo blight (HB)] × black A 55 [dominant I gene resistance to bean common mosaic potyvirus] and to map genes or QTL (quantitative trait loci) for resistance to CBB, HB, BCMV (bean common mosaic virus), and BCMNV (bean common mosaic necrosis virus) diseases. The RI lines were evaluated for resistance to leaf and pod reactions to Xanthomonas campestris pv. phaseoli (Xcp) (Smith Dye) strain EK-11, leaf reactions to two Pseudomonas syringae pv. phaseolicola (Psp) (Burkholder) Young et al. (1978) strains HB16 and 83-Sc2A, and BCMV strain US-5 and BCMNV strain NL-3. The linkage map spanned 755 cM, including 90 markers consisting of 87 RAPD markers, one sequence characterized amplified region (SCAR), the I gene, and a gene for hypersensitive resistance to HB 83-Sc2A. These were grouped into 11 linkage groups (LG) corresponding to the 11 linkage groups in the common bean integrated genetic map. A major gene and QTL for leaf resistance to HB were mapped for the first time. Three QTL for leaf reactions to HB16 were found on linkage groups 3, 5, and 10. Four regions on linkage groups 2, 4, 5, and 9, were significantly associated with leaf reactions to HB strain 83-Sc2A. The gene controlling the hypersensitive reaction to HB 83-Sc2A mapped to the same region as the QTL on LG 4. The I locus for resistance to BCMV and BCMNV was mapped to LG 2 at about 1.4 cM from RAPD marker A10.1750. Five and four markers were significantly associated with QTL for resistance to CBB in leaves and pods, respectively, with four of them associated with resistance in both plant organs. A marker locus was discovered on LG 10, W10.550, which could account for 44% and 41% of the phenotypic variation for CBB resistance in leaves and pods, respectively. QTL for resistance in pod to CBB, leaf resistance to HB, and the I gene were linked on LG 2.

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Saqib, Muhammad, Simon R. Ellwood, Roger A. C. Jones, and Michael G. K. Jones. "Resistance to Subterranean clover mottle virus in Medicago truncatula and genetic mapping of a resistance locus." Crop and Pasture Science 60, no. 5 (2009): 480. http://dx.doi.org/10.1071/cp08373.

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Subterranean clover mottle virus (SCMoV), which causes an important disease of annual clover pastures, was inoculated to the annual pasture legume Medicago truncatula, a model legume species used to help understand legume genome structure and function. Two hundred and nine accessions representing the core collection of M. truncatula were inoculated with infective sap containing SCMoV to determine their disease phenotypes. Forty-two of these accessions remained uninfected systemically and so were potentially resistant to the virus. Accession DZA315.16 developed a localised hypersensitive resistance reaction. In an F8 mapping population from a cross between the susceptible parent Jemalong 6/A17 and resistant accession DZA315.16, a total of 166 F8 recombinant inbred lines (RILs) were phenotyped for resistance and susceptibility to SCMoV. Resistant and susceptible lines showed parental phenotypic responses: 84 were susceptible and 82 were resistant, suggesting presence of a single resistance (R) gene. The phenotypic data were combined with genotypic data (76 polymorphic molecular markers) for this RIL population to provide a framework map. Genetic analysis located a single resistance locus termed RSCMoV1 on the long arm of chromosome 6. These results provide a basis for fine mapping the RSCMoV1 gene.

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Heist, E. P., D. Zaitlin, D. L. Funnell, W. C. Nesmith, and C. L. Schardl. "Necrotic Lesion Resistance Induced by Peronospora tabacina on Leaves of Nicotiana obtusifolia." Phytopathology® 94, no. 11 (November 2004): 1178–88. http://dx.doi.org/10.1094/phyto.2004.94.11.1178.

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Infection of Nicotiana obtusifolia plant introduction (PI) #555573 by the downy mildew pathogen Peronospora tabacina resulted in a compatible interaction, in which P. tabacina penetrated and freely colonized host leaf tissue. This interaction became incompatible 5 to 6 days later, with the appearance of necrotic lesions (NLs) and inhibition of pathogen growth and subsequent sporulation. NL development depended upon the presence of P. tabacina in host tissue, was not due to the effects of other microbes, and occurred co-incident in time with the pathogen's ability to produce asexual sporangia on a susceptible N. obtusifolia genotype. Inhibition of the necrotic response by CoCl2 (a calcium channel blocker) and pathogen-induced transcription of a defense-related gene (PR-1a) suggested that necrosis was due to hypersensitive cell death in the host. In contrast, N. obtusifolia PI#555543 did not exhibit hypersensitivity upon infection by P. tabacina, but rather developed characteristic symptoms of tobacco blue mold disease: chlorotic lesions accompanied by abundant pathogen sporulation. Disease reactions scored on PI#555573 × PI#555543 F2 progeny inoculated with P. tabacina sporangia indicated that the resistance phenotype was due to the action of a single gene from N. obtusifolia PI#555573, which we have named Rpt1. To date, Rpt1 is the only gene known to confer a hypersensitive response (HR) to P. tabacina infection in any species of Nicotiana. A survey of wild N. obtusifolia revealed that the HR to P. tabacina was expressed in the progeny of 7 of 21 (33%) plants collected in southern Arizona, but not in the progeny of plants originating from Death Valley National Park in California and the Big Bend National Park in west Texas.

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