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Статті в журналах з теми "Hypersensitive disease resistance"
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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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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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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.
Повний текст джерелаАнотація:
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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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.
Повний текст джерелаАнотація:
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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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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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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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.
Повний текст джерелаАнотація:
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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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.
Повний текст джерелаАнотація:
: 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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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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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.
Повний текст джерелаАнотація:
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.
Дисертації з теми "Hypersensitive disease resistance"
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Mahmood, Hamida. "Computational mining for terminator-like genes in soybean." Thesis, Kansas State University, 2016. http://hdl.handle.net/2097/32724.
Повний текст джерелаАнотація:
Master of ScienceGenetics Interdepartmental Program - Plant Pathology
Frank F. White
Sanzhen Liu
Plants and bacterial pathogens are in constant co-evolution to survive and sustain the next generation. Plants have two well-characterized levels of active defense -pathogens-associated molecular patterns (PAMPs)-triggered immunity (PTI) and effectors-triggered immunity (ETI). Some plants that are hosts for bacterial pathogens employing type three secretion system transcription activator-like (TAL) effectors have evolved a unique form of ETI, namely TAL effector-mediated ETI. TAL effectors induce expression of specific disease susceptibility (S) genes. Rice and pepper have evolved resistance genes termed terminator (T) genes, which have promoters that bind TAL effectors and, upon expression of the T gene, elicit a hypersensitive reaction (HR) and cell death. Only five T genes have been cloned, and the origin of most T genes is unknown. To determine the presence of candidate T genes in other plants species, a bioinformatics-based mining was designed. The basic approach utilized three structural features common to four terminator genes: a short trans-membrane domain, a secretion signal domain, and a length of <200 amino acid residues. Soybean was chosen as the test plant species, and 161 genes were retrieved that fulfilled the three parameters using R and Perl software programs. Further, functional annotation of candidate genes was conducted by comparisons to genes in public databases. Major classes of proteins found included unique and hypothetical, defense/stress/oxidative stress associated, DNA-binding, kinases, transferases, hydrolases, effector-related tRNA splicing, and F- box domain proteins. The potential T genes will serve as candidates for experimental validation and new resources for durable resistance strategies in crop species.
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Christopher, Stephen James. "Plant-pathogen interactions: turnip crinkle virus suppression of the hypersensitive response in arabidopsis thaliana." Link to electronic thesis, 2003. http://www.wpi.edu/Pubs/ETD/Available/etd-0429103-084755.
Повний текст джерелаАнотація:
Thesis (M.S.)--Worcester Polytechnic Institute.Keywords: Turnip crinkle virus; arabidopsis; thaliana; TCV; avrRpt2; avrRpm1; avrRps4; systemic acquired resistance; virulence; Avr gene; R gene; pseudomonas syringae. Includes bibliographical references (p. 60-66).
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Unver, Turgay. "Detection And Characterization Of Plant Genes Involved In Various Biotic And Abiotic Stress Conditions Using Ddrt-pcr And Isolation Of Interacting Proteins." Phd thesis, METU, 2008. http://etd.lib.metu.edu.tr/upload/12609805/index.pdf.
Повний текст джерелаАнотація:
The main objective of this thesis dissertation is functionally characterizing the genes involved in biotic and abiotic stresses of plants at molecular level. Previously, upon pathogen attack Rad6 gene expression was found to be changed in wheat and barley plants. To functionally characterize the Rad6 gene, VIGS (Virus induced gene silencing) system was used. HR (Hypersensitive response) like symptoms was detected in every silenced barley and wheat plants. To figure out, transcriptomes and proteomes of Rad6 silenced plants were analyzed. 2-D PAGE analysis was also performed on silenced and control wheat plants. No pathogen growth was observed in Rad6 silenced barley lines. Additionally, the susceptible wild type Arabidopsis plants showed resistant phenotype when any of the Rad6 gene copies is mutated. This suggests that Rad6 gene has a negative regulatory role in plant disease resistance which was proved for the first time. Yeast two hybrid protein interaction study suggests that RAD6 carrying out its function by interacting with SGT1 protein and regulating resistance related genes. It has been first time reported in this thesis that E2 (Ubiquitin conjugating enzyme) takes role in plant disease resistance.
Boron which is the other consideration in the scope of thesis as an abiotic stress factor at a very limited amount is necessary for the normal development of plants. This study is conducted on highly boron tolerant Gypsophila perfoliata L. collected from a location in the boron mining area. The plant samples were tested in the presence of high boron (35 mg/kg) concentrations. The transcriptomes of the plant samples treated with the excess levels of boron to that of the samples grown under normal concentration were compared using differential display PCR method. Thirty bands showing differential expression levels at varying time points were analyzed. 18 of them were confirmed via qRT-PCR.
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CHEN, Jian. "Assessment of nitric oxide signaling functions during the plant hypersensitive disease resistance response." Doctoral thesis, 2014. http://hdl.handle.net/11562/720970.
Повний текст джерелаАнотація:
In pianta, ossido nitrico (NO) gioca un ruolo cruciale nel segnale di difesa in risposta all’ infezione causata da batteri patogeni.
Il segnale NO può essere mediato dalle sue dirette interazioni con molecole target, per esempio tramite modificazioni post-traduzionali, ma questo è pensato per le cellule animali, il segnale NO può essere anche usato come secondo messaggero cGMP (guanosina 3’,5’-monofosfato ciclico) in particolare per regolare la difesa del gene d’espressione.
Benché, il ruolo di NO sia stato dimostrato durante l’HR, è ancora molto discusso, probabilmente perché i metodi di misurazione non sono del tutto specifici.
Allo stesso modo, la rivelazione di cGMP in piante fino adesso, è stata basata su metodi che spesso illustrano bassa sensibilità e velocità.
In più, è dovuto alla mancanza d’ identificazione d’ enzimi responsabili al metabolismo di cGMP; fino ad ora, il suo ruolo è stato ricercato solo attraverso l’ uso di composti farmacologici che raramente aumentano la domanda alla specificità di risposta.
In questo studio, abbiamo confermato che NO è prodotto specificamente durante l’incompatibile interazione di un metodo chemoluminescente e che NO comporta la produzione principale di nitrito come substrato e richiede NR come altra risorsa(e) ancora non identificata.
Inoltre, i metodi basati sull’alta sensibilità e alta velocità della tecnologia AlphaSceen erano applicati con successo in pianta a dimostrare la localizzazione locale di NO e l’aumento distale del livello cGMP in risposta ai patogeni avirulenti.
La caratterizzazione della pianta transgenica Arabidopsis thaliana espressa in guanilato ciclasi (GC) solubile di mammifero mostrava che queste piante accumulavano alti livelli costitutivi di cGMP paragonato alle piante WT e illustravano un’ espressione alterata di acido salicilico dipendente dalle difese geniche correlate con perdita stabile acquisita del sistema di resistenza, mentre mostrano una normale resistenza e una morte cellulare ipersensibile a livello locale.
Infine, nelle linee GC, il percorso SA-dipendente sembra essere compromesso in favore delle risposte jasmonate-dipendenti , suggerendo a cGMP un ruolo da interruttore per la regolazione ormonale .In plants, nitric oxide (NO) plays a crucial role in mediating defense signal in response to infection by bacterial pathogens. NO signal can be mediated by its direct interaction with target molecules, via post-translational modifications for instance, but it is believed that, like in animal cells, NO signal can also be relay by the second messenger cGMP (cyclic guanosine 3',5'-monophosphate) in particular to regulate defense gene expression. Despite the demonstration of its role during the HR, the detection of NO is still highly debated, mainly because its measurement methods are not fully specific. In the same way, cGMP detection in plants until now has been based on methods that often display a low sensitivity and a low throughput. In addition, due to the lack of identification of the enzymes responsible for cGMP metabolism, until now, the role of cGMP has been investigated only with the use of pharmacological compounds that sometimes raise the question about response specificity. In this study, we thus confirmed that NO is produced specifically during the incompatible interaction thanks to a chemiluminescence-based method and that NO production involves mainly nitrite as substrate and requires NR as well as other source(s) still unidentified. Moreover, a highly sensitive and with high throughput method based on AlphaScreen technology was successfully applied in plants to demonstrate the NO-dependent local and distal increase of cGMP level in response to avirulent pathogens. The characterization of transgenic Arabidopsis thaliana plants expressing the mammalian soluble guanylate cyclase (GC) showed that these plants accumulate high constitutive levels of cGMP compared with WT plants and display an altered expression of salicylic acid-dependent defence genes correlated with the loss of systemic acquired resistance establishment, while they show a normal resistance and hypersensitive cell death at local level. Moreover, in GC lines, SA-dependent pathway seems to be compromised in favour of jasmonate-dependent responses, suggesting a role for cGMP in regulating the hormonal switch.
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"A novel simple extracellular leucine-rich repeat (eLRR) domain protein from rice (OsLRR1) enters the endosomal pathway and interacts with the hypersensitive induced reaction protein 1 (OsHIR1)." Thesis, 2009. http://library.cuhk.edu.hk/record=b6074981.
Повний текст джерелаАнотація:
Receptor-like protein kinases (RLKs) containing an extracellular leucine-rich-repeat (eLRR) domain, a transmembrane domain, and a cytoplasmic kinase domain play important roles in plant disease resistance. Simple eLRR domain proteins structurally resembling the extracellular portion of the RLKs may also participate in signaling transduction and plant defense response. Yet the molecular mechanisms and subcellular localization in regulating plant disease resistance of these simple eLRR domain proteins are still largely unclear. We provided the first experimental evidence to demonstrate the endosomal localization and trafficking of a novel simple eLRR domain protein (OsLRR1) in the endosomal pathway, using both confocal and electron microscopy. Yeast 2-hybrid and in vitro pull-down assays show that OsLRR1 interacts with the rice hypersensitive induced response protein 1 (OsHIR1) which is localized on plasma membrane. The interaction between LRR1 and HIR1 homologs was shown to be highly conserved among different plant species, suggesting a close functional relationship between the two proteins. The function of OsLRR1 in plant defense response was examined by gain-of-function tests using transgenic Arabidopsis thaliana. The protective effects of OsLRR1 against bacterial pathogen infection were shown by the alleviating of disease symptoms, lowering of pathogen titers, and higher expression of defense marker genes.Zhou, Liang.
Adviser: Hon Ming Lam.
Source: Dissertation Abstracts International, Volume: 73-01, Section: B, page: .
Thesis (Ph.D.)--Chinese University of Hong Kong, 2009.
Includes bibliographical references (leaves 90-107).
Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web.
Electronic reproduction. [Ann Arbor, MI] : ProQuest Information and Learning, [201-] System requirements: Adobe Acrobat Reader. Available via World Wide Web.
Abstract also in Chinese.
Книги з теми "Hypersensitive disease resistance"
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J, Novacky A., ed. The hypersensitive reaction in plants to pathogens: A resistance phenomenon /R.N. Goodman and A.J. Novacky. St. Paul, Minn: APS Press, 1994.
Знайти повний текст джерелаЧастини книг з теми "Hypersensitive disease resistance"
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Delledonne, M., Y. Xia, R. A. Dixon, C. Lorenzoni, and C. Lamb. "Nitric oxide signalling in the plant hypersensitive disease resistance response." In Developments in Plant Breeding, 127–33. Dordrecht: Springer Netherlands, 1999. http://dx.doi.org/10.1007/978-94-011-4475-9_15.
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Chen, Jian, Diana Bellin, and Elodie Vandelle. "Measurement of Cyclic GMP During Plant Hypersensitive Disease Resistance Response." In Methods in Molecular Biology, 143–51. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7668-3_13.
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Alvarez, María Elena. "Salicylic acid in the machinery of hypersensitive cell death and disease resistance." In Programmed Cell Death in Higher Plants, 185–98. Dordrecht: Springer Netherlands, 2000. http://dx.doi.org/10.1007/978-94-010-0934-8_14.
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Jabs, Thorsten, and Alan J. Slusarenko. "The Hypersensitive Response." In Mechanisms of Resistance to Plant Diseases, 279–323. Dordrecht: Springer Netherlands, 2000. http://dx.doi.org/10.1007/978-94-011-3937-3_9.
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Vandelle, Elodie, Tengfang Ling, Zahra Imanifard, Ruitao Liu, Massimo Delledonne, and Diana Bellin. "Nitric Oxide Signaling during the Hypersensitive Disease Resistance Response." In Advances in Botanical Research, 219–43. Elsevier, 2016. http://dx.doi.org/10.1016/bs.abr.2015.10.013.
Повний текст джерелаЗвіти організацій з теми "Hypersensitive disease resistance"
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Sessa, Guido, and Gregory Martin. A functional genomics approach to dissect resistance of tomato to bacterial spot disease. United States Department of Agriculture, January 2004. http://dx.doi.org/10.32747/2004.7695876.bard.
Повний текст джерелаАнотація:
The research problem. Bacterial spot disease in tomato is of great economic importance worldwide and it is particularly severe in warm and moist areas affecting yield and quality of tomato fruits. Causal agent of spot disease is the Gram-negative bacterium Xanthomonas campestris pv. vesicatoria (Xcv), which can be a contaminant on tomato seeds, or survive in plant debris and in association with certain weeds. Despite the economic significance of spot disease, plant protection against Xcvby cultural practices and chemical control have so far proven unsuccessful. In addition, breeding for resistance to bacterial spot in tomato has been undermined by the genetic complexity of the available sources of resistance and by the multiple races of the pathogen. Genetic resistance to specific Xcvraces have been identified in tomato lines that develop a hypersensitive response and additional defense responses upon bacterial challenge. Central goals of this research were: 1. To identify plant genes involved in signaling and defense responses that result in the onset of resistance. 2. To characterize molecular properties and mode of action of bacterial proteins, which function as avirulence or virulence factors during the interaction between Xcvand resistant or susceptible tomato plants, respectively. Our main achievements during this research program are in three major areas: 1. Identification of differentially expressed genes during the resistance response of tomato to Xcvrace T3. A combination of suppression subtractive hybridization and microarray analysis identified a large set of tomato genes that are induced or repressed during the response of resistant plants to avirulent XcvT3 bacteria. These genes were grouped in clusters based on coordinate expression kinetics, and classified into over 20 functional classes. Among them we identified genes that are directly modulated by expression of the type III effector protein AvrXv3 and genes that are induced also during the tomato resistance response to Pseudomonas syringae pv. tomato. 2. Characterization of molecular and biochemical properties of the tomato LeMPK3MAP kinase. A detailed molecular and biochemical analysis was performed for LeMPK3 MAP kinase, which was among the genes induced by XcvT3 in resistant tomato plants. LeMPK3 was induced at the mRNA level by different pathogens, elicitors, and wounding, but not by defense-related plant hormones. Moreover, an induction of LeMPK3 kinase activity was observed in resistant tomato plants upon Xcvinfection. LeMPK3 was biochemically defined as a dual-specificity MAP kinase, and extensively characterized in vitro in terms of kinase activity, sites and mechanism of autophosphorylation, divalent cation preference, Kₘand Vₘₐₓ values for ATP. 3. Characteriztion of molecular properties of the Xcveffector protein AvrRxv. The avirulence gene avrRxvis involved in the genetic interaction that determines tomato resistance to Xcvrace T1. We found that AvrRxv functions inside the plant cell, localizes to the cytoplasm, and is sufficient to confer avirulence to virulent Xcvstrains. In addition, we showed that the AvrRxv cysteine protease catalytic core is essential for host recognition. Finally, insights into cellular processes activated by AvrRxv expression in resistant plants were obtained by microarray analysis of 8,600 tomato genes. Scientific and agricultural significance: The findings of these activities depict a comprehensive and detailed picture of cellular processes taking place during the onset of tomato resistance to Xcv. In this research, a large pool of genes, which may be involved in the control and execution of plant defense responses, was identified and the stage is set for the dissection of signaling pathways specifically triggered by Xcv.
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Sessa, Guido, та Gregory Martin. MAP kinase cascades activated by SlMAPKKKε and their involvement in tomato resistance to bacterial pathogens. United States Department of Agriculture, січень 2012. http://dx.doi.org/10.32747/2012.7699834.bard.
Повний текст джерелаАнотація:
The research problem: Pseudomonas syringae pv. tomato (Pst) and Xanthomonas campestrispv. vesicatoria (Xcv) are the causal agents of tomato bacterial speck and spot diseases, respectively. These pathogens colonize the aerial parts of the plant and cause economically important losses to tomato yield worldwide. Control of speck and spot diseases by cultural practices or chemicals is not effective and genetic sources of resistance are very limited. In previous research supported by BARD, by gene expression profiling we identified signaling components involved in resistance to Xcvstrains. Follow up experiments revealed that a tomato gene encoding a MAP kinase kinase kinase (MAPKKKe) is required for resistance to Xcvand Pststrains. Goals: Central goal of this research was to investigate the molecular mechanisms by which MAPKKKεand associated MAP kinase cascades regulate host resistance. Specific objectives were to: 1. Determine whether MAPKKKεplays a broad role in defense signaling in plants; 2. Identify components of MAP kinase cascades acting downstream of MAPKKKε; 3. Determine the role of phosphorylation-related events in the function of MAPKKKε; 4. Isolate proteins directly activated by MAPKKKε-associatedMAPK modules. Our main achievements during this research program are in the following major areas: 1. Characterization of MAPKKKεas a positive regulator of cell death and dissection of downstream MAP kinase cascades (Melech-Bonfil et al., 2010; Melech-Bonfil and Sessa, 2011). The MAPKKKεgene was found to be required for tomato resistance to Xcvand Pstbacterial strains and for hypersensitive response cell death triggered by different R gene/effector gene pairs. In addition, overexpression analysis demonstrated that MAPKKKεis a positive regulator of cell death, whose activity depends on an intact kinase catalytic domain. Epistatic experiments delineated a signaling cascade downstream of MAPKKKεand identified SIPKK as a negative regulator of MAPKKKε-mediated cell death. Finally, genes encoding MAP kinase components downstream of MAPKKKεwere shown to contribute to tomato resistance to Xcv. 2. Identification of tomato proteins that interact with MAPKKKεand play a role in plant immunity (Oh et al., 2011). We identified proteins that interact with MAPKKKε. Among them, the 14-3-3 protein TFT7 was required for cell death mediated by several R proteins. In addition, TFT7 interacted with the MAPKK SlMKK2 and formed homodimersin vivo. Thus, TFT7 is proposed to recruit SlMKK2 and MAPKKK client proteins for efficient signal transfer. 3. Development of a chemical genetic approach to identify substrates of MAPKKKε-activated MAP kinase cascades (Salomon et al., 2009, 2011). This approach is based on engineering the kinase of interest to accept unnatural ATP analogs. For its implementation to identify substrates of MAPKKKε-activated MAP kinase modules, we sensitized the tomato MAP kinase SlMPK3 to ATP analogs and verified its ability to use them as phosphodonors. By using the sensitized SlMPK3 and radiolabeled N6(benzyl)ATP it should be possible to tag direct substrates of this kinase. 4. Development of methods to study immunity triggered by pathogen-associated molecular patterns (PAMPs) in tomato and N. benthamiana plants (Kim et al., 2009; Nguyen et al. 2010). We developed protocols for measuring various PTI-associatedphenotypes, including bacterial populations after pretreatment of leaves with PAMPs, induction of reporter genes, callose deposition at the cell wall, activation of MAP kinases, and a luciferase-based reporter system for use in protoplasts. Scientific and agricultural significance: Our research activities discovered and characterized a signal transduction pathway mediating plant immunity to bacterial pathogens. Increased understanding of molecular mechanisms of immunity will allow them to be manipulated by both molecular breeding and genetic engineering to produce plants with enhanced natural defense against disease. In addition, we successfully developed new biochemical and molecular methods that can be implemented in the study of plant immunity and other aspects of plant biology.
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Coplin, David L., Shulamit Manulis, and Isaac Barash. roles Hrp-dependent effector proteins and hrp gene regulation as determinants of virulence and host-specificity in Erwinia stewartii and E. herbicola pvs. gypsophilae and betae. United States Department of Agriculture, June 2005. http://dx.doi.org/10.32747/2005.7587216.bard.
Повний текст джерелаАнотація:
Gram-negative plant pathogenic bacteria employ specialized type-III secretion systems (TTSS) to deliver an arsenal of pathogenicity proteins directly into host cells. These secretion systems are encoded by hrp genes (for hypersensitive response and pathogenicity) and the effector proteins by so-called dsp or avr genes. The functions of effectors are to enable bacterial multiplication by damaging host cells and/or by blocking host defenses. We characterized essential hrp gene clusters in the Stewart's Wilt of maize pathogen, Pantoea stewartii subsp. stewartii (Pnss; formerly Erwinia stewartii) and the gall-forming bacterium, Pantoea agglomerans (formerly Erwinia herbicola) pvs. gypsophilae (Pag) and betae (Pab). We proposed that the virulence and host specificity of these pathogens is a function of a) the perception of specific host signals resulting in bacterial hrp gene expression and b) the action of specialized signal proteins (i.e. Hrp effectors) delivered into the plant cell. The specific objectives of the proposal were: 1) How is the expression of the hrp and effector genes regulated in response to host cell contact and the apoplastic environment? 2) What additional effector proteins are involved in pathogenicity? 3) Do the presently known Pantoea effector proteins enter host cells? 4) What host proteins interact with these effectors? We characterized the components of the hrp regulatory cascade (HrpXY ->7 HrpS ->7 HrpL ->7 hrp promoters), showed that they are conserved in both Pnss and Fag, and discovered that the regulation of the hrpS promoter (hrpSp) may be a key point in integrating apoplastic signals. We also analyzed the promoters recognized by HrpL and demonstrated the relationship between their composition and efficiency. Moreover, we showed that promoter strength can influence disease expression. In Pnss, we found that the HrpXY two-component signal system may sense the metabolic status of the bacterium and is required for full hrp gene expression in planta. In both species, acyl-homoserine lactone-mediated quorum sensing may also regulate epiphytic fitness and/or pathogenicity. A common Hrp effector protein, DspE/WtsE, is conserved and required for virulence of both species. When introduced into corn cells, Pnss WtsE protein caused water-soaked lesions. In other plants, it either caused cell death or acted as an Avr determinant. Using a yeast- two-hybrid system, WtsE was shown to interact with a number of maize signal transduction proteins that are likely to have roles in either programmed cell death or disease resistance. In Pag and Pab, we have characterized the effector proteins HsvG, HsvB and PthG. HsvG and HsvB are homologous proteins that determine host specificity of Pag and Pab on gypsophila and beet, respectively. Both possess a transcriptional activation domain that functions in yeast. PthG was found to act as an Avr determinant on multiple beet species, but was required for virulence on gypsophila. In addition, we demonstrated that PthG acts within the host cell. Additional effector genes have been characterized on the pathogenicity plasmid, pPATHₚₐg, in Pag. A screen for HrpL- regulated genes in Pnsspointed up 18 candidate effector proteins and four of these were required for full virulence. It is now well established that the virulence of Gram-negative plant pathogenic bacteria is governed by Hrp-dependent effector proteins. However; the mode of action of many effectors is still unresolved. This BARD supported research will significantly contribute to the understanding of how Hrp effectors operate in Pantoea spp. and how they control host specificity and affect symptom production. This may lead to novel approaches for genetically engineering plants resistant to a wide range of bacterial pathogens by inactivating the Hrp effectors with "plantabodies" or modifying their receptors, thereby blocking the induction of the susceptible response. Alternatively, innovative technologies could be used to interfere with the Hrp regulatory cascade by blocking a critical step or mimicking plant or quorum sensing signals.
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Dickman, Martin B., and Oded Yarden. Genetic and chemical intervention in ROS signaling pathways affecting development and pathogenicity of Sclerotinia sclerotiorum. United States Department of Agriculture, July 2015. http://dx.doi.org/10.32747/2015.7699866.bard.
Повний текст джерелаАнотація:
Abstract: The long-term goals of our research are to understand the regulation of sclerotial development and pathogenicity in S. sclerotior11111. The focus in this project was on the elucidation of the signaling events and environmental cues involved in the regulation of these processes, utilizing and continuously developing tools our research groups have established and/or adapted for analysis of S. sclerotiorum, Our stated objectives: To take advantage of the recent conceptual (ROS/PPs signaling) and technical (amenability of S. sclerotiorumto manipulations coupled with chemical genomics and next generation sequencing) developments to address and extend our fundamental and potentially applicable knowledge of the following questions concerning the involvement of REDOX signaling and protein dephosphorylation in the regulation of hyphal/sclerotial development and pathogenicity of S. sclerotiorum: (i) How do defects in genes involved in ROS signaling affect S. sclerotiorumdevelopment and pathogenicity? (ii) In what manner do phosphotyrosinephosphatases affect S. sclerotiorumdevelopment and pathogenicity and how are they linked with ROS and other signaling pathways? And (iii) What is the nature of activity of newly identified compounds that affect S. sclerotiori,111 growth? What are the fungal targets and do they interfere with ROS signaling? We have met a significant portion of the specific goals set in our research project. Much of our work has been published. Briefly. we can summarize that: (a) Silencing of SsNox1(NADPHoxidase) expression indicated a central role for this enzyme in both virulence and pathogenic development, while inactivation of the SsNox2 gene resulted in limited sclerotial development, but the organism remained fully pathogenic. (b) A catalase gene (Scatl), whose expression was highly induced during host infection is involved in hyphal growth, branching, sclerotia formation and infection. (c) Protein tyrosine phosphatase l (ptpl) is required for sclerotial development and is involved in fungal infection. (d) Deletion of a superoxidedismutase gene (Sssodl) significantly reduced in virulence on both tomato and tobacco plants yet pathogenicity was mostly restored following supplementation with oxalate. (e) We have participated in comparative genome sequence analysis of S. sclerotiorumand B. cinerea. (f) S. sclerotiorumexhibits a potential switch between biotrophic and necrotrophic lifestyles (g) During plant microbe interactions cell death can occur in both resistant and susceptible events. Non pathogenic fungal mutants S. sclerotior111n also cause a cell death but with opposing results. We investigated PCD in more detail and showed that, although PCD occurs in both circumstances they exhibit distinctly different features. The mutants trigger a restricted cell death phenotype in the host that unexpectedly exhibits markers associated with the plant hypersensitive (resistant) response. Using electron and fluorescence microscopy, chemical effectors and reverse genetics, we have established that this restricted cell death is autophagic. Inhibition of autophagy rescued the non-pathogenic mutant phenotype. These findings indicate that autophagy is a defense response in this interaction Thus the control of cell death, dictated by the plant (autophagy) סr the fungus (apoptosis), is decisive to the outcome of certain plant microbe interactions. In addition to the time and efforts invested towards reaching the specific goals mentioned, both Pls have initiated utilizing (as stated as an objective in our proposal) state of the art RNA-seq tools in order to harness this technology for the study of S. sclerotiorum. The Pls have met twice (in Israel and in the US), in order to discuss .נחd coordinate the research efforts. This included a working visit at the US Pls laboratory for performing RNA-seq experiments and data analysis as well as working on a joint publication (now published). The work we have performed expands our understanding of the fundamental biology (developmental and pathogenic) of S. sclerotioז111וז. Furthermore, based on our results we have now reached the conclusion that this fungus is not a bona fide necrotroph, but can also display a biotrophic lifestyle at the early phases of infection. The data obtained can eventually serve .נ basis of rational intervention with the disease cycle of this pathogen.