Готові списки джерел за темами / Host disease resistance

Добірка наукової літератури з теми "Host disease resistance"

Автор: Grafiati
Опубліковано: 10 грудня 2022
Оновлено: 29 січня 2023

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Статті в журналах з теми "Host disease resistance"

1

Dixon, G. R. "Interactions of soil nutrient environment, pathogenesis and host resistance." Plant Protection Science 38, SI 1 - 6th Conf EFPP 2002 (January 1, 2002): S87—S94. http://dx.doi.org/10.17221/10326-pps.

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Host plants and soil borne pathogens that attack them exist within an ecological matrix populated by numerous microbial species that may influence the access of pathogenesis. These events are moderated by physical and chemical components of the soil. The impact of inorganic and organic nutrients on pathogenesis and the development of host resistance are discussed in this review using two host – pathogen combinations as examples. Calcium, boron, nitrogen and pH have been demonstrated to affect the processes of resting spore germination, host invasion and colonisation in the Plasmodiophora brassicae-Brassica combination that results in clubroot disease. Organic nutrients that have associated biostimulant properties have been demonstrated to influence the development of Pythium ultimum-Brassica combination that results in damping-off disease. This latter combination is affected by the presence of antagonistic microbial flora as demonstrated by increased ATP, extra-cellular enzyme and siderophore production. In both examples there are indications of the manner by which host resistance to pathogenesis may be enhanced by changes to the nutrient status surrounding host plants. These effects are discussed in relation to the development of integrated control strategies that permit disease control with minimal environmental impact.
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2

Alemu, Gadisa. "Wheat Breeding for Disease Resistance: Review." Open Access Journal of Microbiology & Biotechnology 4, no. 2 (2019): 1–10. http://dx.doi.org/10.23880/oajmb-16000142.

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Breeding for disease resistance is a central focus of plant breeding programs, as any successful variety must have the complete package of high yield, disease resistance, agronomic performance, and end - use quality. Wheat breeding is focused on high yield, pathogen resistance and abiotic stress tolerance. Among diseases of wheat yellow rust, stem rust, and leaf rust are the most damaging diseases of wheat and other small grain cereals . Disease resistance in wheat breeding with one exception, the diseases of wheat that is important because of their effect on yield. Resistance to all diseases together can is important to avoid an unexpected loss in effectiveness of the resistance of a cu ltivar to a major disease. The genetic resistance to stem rust, leaf rust and yellow rust can be characterized as qualitative and quantitative resistances. Vertical resistance is specific to pathogen isolates based on single or very few genes. Race - specifi c is used to describe resistance that interacts differentially with pathogen races. Quantitative resistance is defined as resistance that varies in continuous way between the various phenotypes of the host population, from almost imperceptible to quite str ong. With the need to accelerate the development of improved varieties, genomics - assisted breeding is becoming an important tool in breeding programs. With marker - assisted selection, there has been success in breeding for disease resistance. Generally, bre eding programs have successfully implemented molecular markers to assist in the development of cultivars with stem, leaf and stripe rust resistance genes. When new rust resistance genes are to be deployed in wheat breeding programs, it unfortunately takes several years before the new sources of resistance will become available in commercial wheat cultivars. This is due to the long process involved in the establishment of pure breeding wheat lines. Biotechnology based techniques are available to accelerate t he breeding process via doubled haploid production.
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3

Jacobs, Jonathan M., and Caitilyn Allen. "Disease Resistance Against a Broad-Host-Range Pathogen." Plant Health Progress 14, no. 1 (January 2013): 32. http://dx.doi.org/10.1094/php-2013-1125-03-rs.

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The bacterial wilt pathogen Ralstonia solanacearum causes major agricultural losses on many crop hosts worldwide. Resistance breeding is the best way to control bacterial wilt disease, but the biological basis for bacterial wilt resistance is unknown. We found that R. solanacearum uses an AvrE-family, Type III-secreted effector called PopS to overcome plant defenses and cause disease on tomato. Orthologs of PopS are widely conserved across distinct classes of plant pathogenic bacteria and could provide novel, durable targets for resistance. Accepted for publication 25 September 2013. Published 25 November 2013.
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4

Friedl, Karl E. "RE: Does host energy metabolism moderate disease resistance?" Journal of Infection 76, no. 2 (February 2018): 211–12. http://dx.doi.org/10.1016/j.jinf.2017.09.017.

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5

Sutherland, M. L., L. Mittempergher, and C. M. Brasier. "Control of Dutch elm disease by induced host resistance." Forest Pathology 25, no. 6-7 (November 1995): 307–15. http://dx.doi.org/10.1111/j.1439-0329.1995.tb01346.x.

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6

Kim, Bong-Suk, Elizabeth French, Denise Caldwell, Emily J. Harrington, and Anjali S. Iyer-Pascuzzi. "Bacterial wilt disease: Host resistance and pathogen virulence mechanisms." Physiological and Molecular Plant Pathology 95 (July 2016): 37–43. http://dx.doi.org/10.1016/j.pmpp.2016.02.007.

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7

Pilla-Moffett, Danielle, Matthew F. Barber, Gregory A. Taylor, and Jörn Coers. "Interferon-Inducible GTPases in Host Resistance, Inflammation and Disease." Journal of Molecular Biology 428, no. 17 (August 2016): 3495–513. http://dx.doi.org/10.1016/j.jmb.2016.04.032.

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8

Omara, Reda Ibrahim, Said Mohamed Kamel, Sherif Mohamed El-Ganainy, Ramadan Ahmed Arafa, Yasser Sabry Mostafa, Saad Abdulrahman Alamri, Sulaiman A. Alrumman, Mohamed Hashem, and Mohsen Mohamed Elsharkawy. "Host Resistance to Uromyces appendiculatus in Common Bean Genotypes." Plants 11, no. 5 (February 25, 2022): 628. http://dx.doi.org/10.3390/plants11050628.

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Rust, induced by the fungus Uromyces appendiculatus, is one of the most serious bean diseases. The involved mechanisms in rust resistance were evaluated in 10 common bean genotypes during the 2019/2020 and 2020/2021 growing seasons. The disease parameters such as final rust severity (FRS%), area under the disease progress curve (AUDPC) and disease increase rate (r-value) were lower in the resistant genotypes than in highly susceptible genotypes. Biochemical compounds such as total phenols and the activity of antioxidant enzymes such as catalase, peroxidase and polyphenol oxidase were increased in the resistant genotypes compared to susceptible genotypes. In the resistance genotypes, the levels of oxidative stress markers such as hydrogen peroxide (H2O2) and superoxide (O2•−) increased dramatically after infection. The electrolyte leakage percentage (EL%), was found to be much greater in susceptible genotypes than resistant genotypes. The resistant gene SA14, which was found in genotypes Nebraska and Calypso at 800 bp, had an adequate level of resistance to bean rust with high grain yield potential. After infection, the transcriptions levels of 1,3-D-glucanases and phenylalanine ammonia lyase) were higher in the resistant genotypes than susceptible genotypes. In conclusion, the resistant genotypes successfully displayed desirable agronomic traits and promising expectations in breeding programs for improving management strategies of common bean rust disease. The resistance was mediated by antioxidant enzymes, phenolic compounds, and defense gene expressions, as well as the resistant gene SA14.
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9

de Silva, Kumudika, Douglas Begg, Karren Plain, Auriol Purdie, Satoko Kawaji, Navneet Dhand, and Richard Whittington. "Early biomarkers of resistance and susceptibility to mycobacterial disease (160.1)." Journal of Immunology 188, no. 1_Supplement (May 1, 2012): 160.1. http://dx.doi.org/10.4049/jimmunol.188.supp.160.1.

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Abstract Mycobacterial diseases such as tuberculosis and paratuberculosis continue to be of serious health and economic concern to humans and livestock globally. Lack of knowledge on the nature of the protective immune response as well as immunological markers of disease susceptibility and latency hamper the development of effective vaccines and other therapies. The use of a well-characterised ruminant infection model enabled us to follow the host response to mycobacterial challenge from the time of exposure until manifestation of clinical disease in a natural host. This study (30 controls and 58 challenged in 2 trials) tracked cellular and humoral responses, and quantity of mycobacterial shedding, for up to 30 months post challenge in sheep. Infection was defined as the presence of viable organisms in tissue sections taken at necropsy. The IFNγ response increased after exposure regardless of disease outcome. Parameters measured could distinguish severely diseased animals from those that had been exposed but were uninfected. Infectious or severely diseased animals were more likely to have a lower IFNγ response early (4 months post exposure) compared to exposed uninfected animals. This latter group were also more likely to have an elevated early IL-10 response. These studies demonstrate the complexity of the immune response to pathogenic mycobacteria and illustrate the fact that measurement of a single immunological parameter is insufficient to determine the outcome of disease.
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10

Kayihan, Gögçe C., C. Dana Nelson, Dudley A. Huber, Henry V. Amerson, Timothy L. White, and John M. Davis. "Clonal evaluation for fusiform rust disease resistance: effects of pathogen virulence and disease escape." Canadian Journal of Forest Research 40, no. 6 (June 2010): 1042–50. http://dx.doi.org/10.1139/x10-045.

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We evaluated the precision of phenotypic classification for fusiform rust resistance of Pinus taeda L. in a clonally propagated population segregating for the pathotype-specific resistance gene Fr1. In all marker-defined Fr1/fr1 clones screened with low complexity or ambient inoculum, marker–trait cosegregation was complete with no exceptions. Uncommon exceptions (4 of 30) in which marker-defined Fr1/fr1 clones screened with high complexity inoculum were diseased were probably due to a low frequency of spores virulent to Fr1 resistance. Marker–trait cosegregation for fr1/fr1 clones was less reliable, as all ramets of a few clones (5 of 29, 3 of 25, and 4 of 16) remained disease-free with low complexity, high complexity, or ambient inoculum, respectively. We termed disease-free fr1/fr1 ramets “escapes”, since the genetics of the host–pathogen interaction predicted them to be diseased. For nonmarker-defined materials, we considered escapes to be disease-free ramets within clones that had at least one diseased ramet. Narrow-sense heritability estimates for escape rate were 29% and 23% for the low and high complexity inocula, respectively, suggesting that genetic variation in the host is an important component of this resistance mechanism.
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Дисертації з теми "Host disease resistance"

1

Shafiei-Adjbisheh, Reza. "Genetic analysis of Arabidopsis non-host disease resistance." Thesis, University of Edinburgh, 2007. http://hdl.handle.net/1842/14381.

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Significant differences were observed among 79 geographically diverse Arabidopsis accessions in response to the wheat powdery mildew pathogen, Blumeria graminis f.sp. tritici (Bgt) and the wheat leaf rust pathogen Puccinia triticina (Ptr). In response to Bgt genotypes classified into two major classes based on the degree of compatibility, Wc-1 an accession from Germany expressed significantly high frequency of penetration. Interestingly, in response to Ptr, a high frequency of guard cell death and sub-stomata vesicle formation (SVF) was observed on Wa-1, an accession from Poland. Attempted Ptr infection induced the production of reaction oxygen intermediates (ROI), nitric oxide, salicylic acid (SA) and camalexin. The expression of SA, jasmonic acid and ROI-dependent genes were also detected. Multiple small-to-medium effect quantitative trait loci (QTL) were identified that govern the expression of NMR in Arabidopsis against Ptr. In response to Bgt, a leaf collapse phenotype was observed in Ler when it was pre-treated with Cytochalasin E, an inhibitor of actin microfilament polymerization. Whereas, Col did not express a similar phenotype. This reaction showed a complicated genetic basis with the involvement of several genes. Our genetic analysis revealed two major QTLs on chromosomes one and three with the existence of episatsis effects. A role for ASYMMETRIC LEAVES1 (AS1) in plant immunity has recently been identified. My experiments showed a conserved regulatory function for NSPHAN, an orthologue of ASI gene in Nicotiana sylvestris when challenged with host and nonhost pathogens. This regulatory gene action remained consistent when the as1 mutant was coupled with key Arabidopsis defence related mutants.
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2

Cotter, Sheena C. "Trade-offs in insect disease resistance." Thesis, University of Stirling, 2002. http://hdl.handle.net/1893/26688.

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The ability to mount an efficient immune response should be an important life-history trait as parasitism can impact upon an individual's fecundity and survival prospects, and hence its fitness. However, immune function is likely to be costly as resources must be divided between many important traits. Whilst many studies have examined host resistance to particular parasite types, fewer have considered general immune responses. Studies that have considered general immune responses tend to do so in vertebrate models. However, the complexity of the vertebrate immune system makes the examination of evolutionary aspects of immune function difficult. Using larvae of the genus Spodoptera (Lepidoptera: Noctuidae) as a model system, this study examines' genetic and phenotypic aspects of innate immunity. The aims were to assess the levels of additive genetic variation maintained in immune traits, to consider possible costs that could maintain this variation, and to assess the role of phenotypic plasticity in ameliorating those costs. A key finding of this study was that high levels of additive genetic variation were maintained in all of the measured Immune traits. Analysis of the genetic correlations between traits revealed potential trade-offs within the immune system and between immune components and body condition. In addition, it was shown that larvae living at high densities invest more in immune function than those living in solitary conditions, suggesting that larvae can minimise the costs of immune function by employing them only when the risk of pathogenesis is high.
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Donnelly, Ruairi. "Eco-evolutionary modelling of infectious disease and host resistance." Thesis, Heriot-Watt University, 2015. http://hdl.handle.net/10399/2914.

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In this work we take an evolutionary invasion analysis approach to modelling evolution and use it to describe the selection pressures underlying epidemiological traits in natural host populations harboring endemic infections. Throughout this work a logistic form for host-birth rate allows for disease dependent population dynamics so that the detrimental e ects of infection can be modelled and we also consider the more neglected detrimental e ect whereby infection is linked to infertility. To begin with we give a theoretical introduction to the framework of adaptive dynamics and illustrate it through the established example of the evolution of parasite virulence. We then extend the results to account for condition dependent virulence which is an interaction between host condition (i.e. host stress) and virulence, that has recently generated much attention from empiricists. Many natural systems are seasonal, potentially leading to seasonal stress, and we show how to conduct a study for seasonal host populations and analyse its role in the evolution of density dependent virulence. We then turn our attention to the evolution of resistance beginning with a perspective on the relationship between investment in acquired immunity and the lifespan of hosts and parasites. In our penultimate chapter we derive explicit expressions for optimal investment in the various modes of resistance for a range of epidemiological scenarios. These expressions are then key to understanding our nal chapter where we elaborate further on the established theory by allowing for parasite diversity. The nal chapter highlights the central role played by speci city in the evolution of host defence. Since our approach throughout has been to build complexity onto a baseline model we conclude our discussion with a short section interpreting established results on the coevolution of virulence and resistance from the perspective of our results on the evolution of virulence and resistance.
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4

Brownlee, Helen Elizabeth. "Host-pathogen interactions in witches's broom disease of cocoa." Thesis, Aberystwyth University, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.333644.

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Cox, Cindy Marie. "Cytogenetic characterization and disease resistance of perennial grasses and disease response to host diversity /." Search for this dissertation online, 2004. http://wwwlib.umi.com/cr/ksu/main.

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6

Edwards, Suzanne Joy. "The mechanism of host resistance in celery to Septoria apiicola (Speg.)." Thesis, University of Liverpool, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.357444.

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Krenz, Jennifer E. "Specificity of quantitatively expressed host resistance to Mycosphaerella graminicola /." Connect to this title online, 2007. http://hdl.handle.net/1957/3813.

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8

Yu, Yong Gang. "Molecular genetic analysis of host resistance to soybean mosaic virus." Diss., Virginia Tech, 1994. http://hdl.handle.net/10919/37253.

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Asea, Godfrey Rox. "Genetic characterization of partial resistance and comparative strategies for improvement of host-resistance to multiple foliar pathogens of maize." Columbus, Ohio : Ohio State University, 2005. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1133833939.

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Sellers, Scott Michael. "A quantitative analysis of Marek's disease virus in relation to host genetic resistance." Thesis, University of Bristol, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.394070.

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Книги з теми "Host disease resistance"

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S, Sadasivam. Molecular host plant resistance to pests. New York: Marcel Dekker, 2003.

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2

Host management in crop pathosystems. New York: Macmillan, 1987.

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3

Vidhyasekaran, P. Fungal pathogenesis in plants and crops: Molecular biology and host defense mechanisms. New York: M. Dekker, 1997.

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4

Flanders, Kathy L. Host plant resistance in Solanum germplasm: An appraisal of resistance to Colorado potato beetle, Potato leafhopper and Potato flea beetle. St.Paul,Minn: Minnesota Agricultural Experiment Station, University of Minnesota, 1992.

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5

Flanders, Kathy Linn. Host plant resistance in Solanum germplasm: An appraisal of resistance to Colorado potato beetle, potato leafhopper and potato flea beetle. St. Paul, Minn: Minnesota Agricultural Experiment Station, University of Minnesota, 1992.

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6

Deverall, Brian J. Defence mechanisms of plants. Cambridge: Cambridge University Press, 2009.

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7

1928-, Day Peter R., Jellis G. J, and British Society for Plant Pathology., eds. Genetics and plant pathogenesis. Oxford [Oxfordshire]: Blackwell Scientific Publications, 1987.

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8

Fungal pathogenesis in plants and crops: Molecular biology and host defense mechanisms. 2nd ed. Boca Raton: CRC Press, 2008.

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9

Or.) International Workshop on the Genetics of Host-Parasite Interactions in Forestry (4th 2011 Eugene. Proceedings of the Fourth International Workshop on the Genetics of Host-Parasite Interactions in Forestry: Disease and insect resistance in forest trees : July 31 to August 5, 2011, Eugene, Oregon, USA. Albany, CA: U.S. Dept. of Agriculture, Forest Service, Pacific Southwest Research Station, 2012.

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10

NATO Advanced Research Workshop on Biology and Molecular Biology of Plant-Pathogen Interactions (1985 Ilminster). Biology and molecular biology of plant-pathogen interactions: Proceedings of the NATO Advanced Research Workshop on Biology and Molecular Biology of Plant-Pathogen Interactions held at Dillington College, Ilminster, U.K., September 1-6, 1985. New York: Springer, 1986.

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Частини книг з теми "Host disease resistance"

1

Saharan, Govind Singh, Naresh K. Mehta, and Prabhu Dayal Meena. "Host Resistance." In Clubroot Disease of Crucifers, 449–543. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-16-2133-8_11.

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Saharan, Govind Singh, Naresh Mehta, and Prabhu Dayal Meena. "Host Resistance." In Downy Mildew Disease of Crucifers: Biology, Ecology and Disease Management, 225–83. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-7500-1_12.

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Saharan, Govind Singh, Naresh K. Mehta, and Prabhu Dayal Meena. "Host Resistance." In Powdery Mildew Disease of Crucifers: Biology, Ecology and Disease Management, 177–295. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-9853-7_7.

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4

Grimsley, N., and J. F. Wang. "Chair’s Perspective: Host Resistance." In Bacterial Wilt Disease, 197–99. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-662-03592-4_29.

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Saharan, Govind Singh, Naresh K. Mehta, and Prabhu Dayal Meena. "Management of Disease Resistance." In Genomics of Crucifer’s Host-Resistance, 505–98. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-16-0862-9_7.

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6

Saharan, Govind Singh, Naresh K. Mehta, and Prabhu Dayal Meena. "Inheritance of Disease Resistance." In Genomics of Crucifer’s Host-Resistance, 195–264. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-16-0862-9_3.

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Saharan, Govind Singh, Naresh K. Mehta, and Prabhu Dayal Meena. "Transfer of Disease Resistance." In Genomics of Crucifer’s Host-Resistance, 265–357. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-16-0862-9_4.

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Ayliffe, Michael, Ming Luo, Justin Faris, and Evans Lagudah. "Disease Resistance." In Wheat Improvement, 341–60. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-90673-3_19.

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AbstractWheat plants are infected by diverse pathogens of economic significance. They include biotrophic pathogens like mildews and rusts that require living plant cells to proliferate. By contrast necrotrophic pathogens that cause diseases such as tan spot, Septoria nodurum blotch and spot blotch require dead or dying cells to acquire nutrients. Pioneering studies in the flax plant-flax rust pathosystem led to the ‘gene-for-gene’ hypothesis which posits that a resistance gene product in the host plant recognizes a corresponding pathogen gene product, resulting in disease resistance. In contrast, necrotrophic wheat pathosystems have an ‘inverse gene-for-gene’ system whereby recognition of a necrotrophic fungal product by a dominant host gene product causes disease susceptibility, and the lack of recognition of this pathogen molecule leads to resistance. More than 300 resistance/susceptibility genes have been identified genetically in wheat and of those cloned the majority encode nucleotide binding, leucine rich repeat immune receptors. Other resistance gene types are also present in wheat, in particular adult plant resistance genes. Advances in mutational genomics and the wheat pan-genome are accelerating causative disease resistance/susceptibility gene discovery. This has enabled multiple disease resistance genes to be engineered as a transgenic gene stack for developing more durable disease resistance in wheat.
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Saharan, Govind Singh, Naresh K. Mehta, and Prabhu Dayal Meena. "Molecular Mechanisms of Disease Resistance." In Molecular Mechanism of Crucifer’s Host-Resistance, 1–75. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-16-1974-8_1.

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Saharan, Govind Singh, Naresh K. Mehta, and Prabhu Dayal Meena. "Biometabolomics of Disease Resistance to." In Molecular Mechanism of Crucifer’s Host-Resistance, 349–494. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-16-1974-8_4.

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Тези доповідей конференцій з теми "Host disease resistance"

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Jonsson, Nicholas Nils. "Evolutionary analysis of host resistance to cattle tick infestation and tick-borne disease in ungulates." In 2016 International Congress of Entomology. Entomological Society of America, 2016. http://dx.doi.org/10.1603/ice.2016.92916.

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McGrath, J. Mitchell, and Suba Nagendran. "Discovery of resistance to seedling disease caused by Rhizoctonia solani AG2-2, description of the host-pathogen interaction, and development of a seedling disease screening nursery." In American Society of Sugar Beet Technologist. ASSBT, 2007. http://dx.doi.org/10.5274/assbt.2007.55.

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Geven, Maartje C. F., Arjen Van Der Horst, Marcel C. M. Rutten, Wilbert Aarnoudse, Nico H. J. Pijls, and Frans N. van de Vosse. "In-Vitro Evaluation of Hot-Film Anemometry Using a Sensor-Tipped Coronary Guide-wire." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176124.

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During coronary catheterization, the epicardial coronary arteries are visually assessed for stenoses on the coronary angiogram. However, the functional significance of disease in the coronary arterial tree, the increased resistance to blood flow, may easily be over- or underestimated by using a 2D projection.
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MAJEED, Huda Zuheir, Firas Nabeeh JAAFAR, Mohammed Twfeek ABID ALHUSAIN, Shatha Zuheir MAJEED, and Nadia Kamil BASHAR. "THE ANTIBACTERIAL EFFECTS OF GREEN TEA EXTRACT ON RESISTANT BACTERIA ISOLATED FROM HUMAN EYE INFECTIONS." In IV.International Scientific Congress of Pure,Appliedand Technological Sciences. Rimar Academy, 2022. http://dx.doi.org/10.47832/minarcongress4-28.

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Ocular infection is a world wide issue especially for public health field which could be a result to its own normal flora due to subjection to external factors (e.g. stress, getting older, hits, surgical operations, systemic diseases and losing commensal flora). Ocular pathogens could be healed by a group of topical antibiotics, but with time, drug resistance had been developed, which more magnified by wrong diagnosis and random use of antibiotics leading to unexpected complications e.g. visual problems, leading to blindness at last . Alternative therapy had been used to treat such infections including plant extracts like Green Tea (Camellia sinensis) . Eye swabs about (50) samples were gathered from people had ocular infections,then biochemical tests diagnosed (30) bacterial isolates. There were (17) isolates (6 isolates of Staphylococcus spp. and 11 isolates were Enterococcus) out of the (30) isolates showed multiple antibiotic resistance to nine antibiotics by disc-diffusion method,there were high complete resistance to Moxifloxacin and Bacitracin, in contrast to Ciprofloxacin and Chloramphenicol. The antibacterial effects of hot water, cold water,Acetone, Ethanol and Methanol Green tea extracts was examined against the (17) multiple antibiotic resistant isolates by agar-well diffusion method using. Only the Ethanol and Methanol green tea extract showed promising results, without any effect of the remaining green tea extracts. Green tea extracts were equal to Ciprofloxacin and Sulphamethoxazole in effectiveness against antibiotic resistant isolates . The (17) isolates were tested for production of biofilm and protease. (12) isolates were biofilm-producer but after subjection to Ethanol Green tea extract changed into non biofilmformer. (13) isolate were protease-producer but after subjection to Ethanol Green tea extract changed into non protease-former. Key words: Eye Swabs, Antibiotic Resistance, Alternative Therapy, Green Tea Extracts, Biofilm and Protease.
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5

Brlansky, R. H. "Update on Huanglongbing Progression and Current Research in Florida." In ASME 2009 Citrus Engineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/cec2009-5501.

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Анотація:
Citrus Huanglongbing (HLB) or citrus greening disease has been in Florida since at least 2005 and has spread to all of the citrus producing regions. The Asian citrus psyllid (Diaphorina citri) is the insect that transmits the suspected causal bacterium which is tentatively named Candidatus Liberibacter asiaticus. Symptoms of the disease are first the yellow shoot (huanglongbing) and the development of the blotchy mottle symptom in the leaves. Mineral deficiency symptoms are often found on infected trees and may mimic normal deficiency symptoms. Fruit on infected trees may be small and lopsided and may abscise prematurely and therefore productivity is reduced. Tree decline eventually occurs. The suspected causal bacterium has not been obtained in pure culture and a polymerase chain reaction (PCR) test along with symptoms, is the only way to verify infected trees. All citrus cultivars appear susceptible. Current management strategies are chemical and biological control to reduced psyllid populations, inspections for infected trees and removal of infected trees to reduce the available pathogen inoculum. Current research on psyllid control, psyllid transmission, symptomology, detection, culturing the causal agent, development of new detection methods, alternative hosts of the psyllid and the causal agent, physiology of the disease, resistant or tolerant cultivar development and more is discussed. HLB is a major problem for citrus production and often limits commercial production. Paper published with permission.
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Звіти організацій з теми "Host disease resistance"

1

Zhao, Bingyu, Saul Burdman, Ronald Walcott, and Gregory E. Welbaum. Control of Bacterial Fruit Blotch of Cucurbits Using the Maize Non-Host Disease Resistance Gene Rxo1. United States Department of Agriculture, September 2013. http://dx.doi.org/10.32747/2013.7699843.bard.

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Анотація:
The specific objectives of this BARD proposal were: (1) To determine whether Rxol can recognize AacavrRxo1 to trigger BFB disease resistance in stable transgenic watermelon plants. (2) To determine the distribution of Aac-avrRxo1 in a global population of Aae and to characterize the biological function of Aac-avrRxo1. (3) To characterize other TIS effectors of Aae and to identify plant R gene(s) that can recognize conserved TIS effectors of this pathogen. Background to the topic: Bacterial fruit blotch (BFB) of cucurbits, caused by Acidovorax avenae subsp. citrulli (Aae), is a devastating disease that affects watermelon (Citrullus lanatus) and melon (Cucumis melo) production worldwide, including both Israel and USA. Two major groups of Aae strains have been classified based on their virulence on host plants, genetics and biochemical properties. Thus far, no effective resistance genes have been identified from cucurbit germplasm. In this project, we assessed the applicability of a non-host disease resistance gene, Rxol, to control BFB in watermelon. We also tried to identify Aae type III secreted (TIS) effectors that can be used as molecular probes to identify novel disease resistance genes in both cucurbits and Nieotianatabaeum. Major conclusions, solutions, achievements: We generated five independent transgenic watermelon (cv. Sugar Babay) plants expressing the Rxol gene. The transgenic plants were evaluated with Aae strains AAC001 and M6 under growth chamber conditions. All transgenic plants were found to be susceptible to both Aae strains. It is possible that watermelon is missing other signaling components that are required for Rxol-mediated disease resistance. In order to screen for novel BFB resistance genes, we inoculated two Aae strains on 60 Nieotiana species. Our disease assay revealed Nicotiana tabaeum is completely resistant to Aae, while its wild relative N. benthamiana is susceptible to Aae. We further demonstrated that Nieotiana benthamiana can be used as a surrogate host for studying the mechanisms of pathogenesis of Aae. We cloned 11 TIS effector genes including the avrRxolhomologues from the genomes of 22 Aae strains collected worldwide. Sequencing analysis revealed that functional avrRxol is conserved in group" but not group I Aae strains. Three effector genes- Aave_1548, Aave_2166 and Aave_2708- possessed the ability to trigger an HR response in N. tabacum when they were transiently expressed by Agrobaeterium. We conclude that N. tabacum carries at least three different non-host resistance genes that can specifically recognize AaeTIS effectors to trigger non-host resistance. Screening 522 cucurbits genotypes with two Aae strains led us to identify two germplasm (P1536473 and P1273650) that are partially resistant to Aae. Interestingly, transient expression of the TIS effector, Aave_1548, in the two germplasms also triggered HR-Iike cell death, which suggests the two lines may carry disease resistance genes that can recognize Aave_1548. Importantly, we also demonstrated that this effector contributes to the virulence of the bacterium in susceptible plants. Therefore, R genes that recognize effector Aave1548 have great potential for breeding for BFB resistance. To better understand the genome diversity of Aae strains, we generated a draft genome sequence of the Israeli Aae strain, M6 (Group I) using Iliumina technology. Comparative analysis of whole genomes of AAC001, and M6 allowed us to identify several effectors genes that differentiate groups I and II. Implications, both scientific and agricultural: The diversity of TIS effectors in group I and II strains of Aae suggests that a subset of effectors could contribute to the host range of group I and II Aae strains. Analysis of these key effectors in a larger Aae population may allow us to predict which cucurbit hosts may be at risk to BFB. Additionally, isolation of tobacco and cucurbit Rgenes that can recognize Aae type III effectors may offer new genetic resources for controlling BFB.
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2

Shtienberg, Dan, William Fry, Amos Dinoor, Thomas Zitter, and Uzi Kafkafi. Reduction in Pesticide Use in Plant Disease Control by Integration of Chemical and Non-Chemical Factors. United States Department of Agriculture, May 1995. http://dx.doi.org/10.32747/1995.7613027.bard.

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The long term goal of this research project was to improve control efficiency of Alternaria diseases while reducing fungicide use, by integration of chemical and non-chemical factors. Non-chemical factors were genotype resistance, age-related resistance and fertilizers. The Specific objectives were: 1) To quantify changes in resistance among genotypes and over time in terms of disease development and specific phases of the disease cycle; 2) To quantify the effects of fertilizers applied to the foliage alone, or in combination with a fungicide, on disease development; 3) To quantify the relative contribution of genotype resistance, age-related resistance and fungicide type to the reduction of disease development; 4) To develop a strategy for integration of chemical and non-chemical factors which will achieve optimal disease suppression. The influence of physiological age of cotton plants and of the individual leaves, on disease incidence and on the rate of lesion expansion of A. macrospora was examined on leaves sampled from the field. Both parameters increased with the physiological age of individual leaves but were not affected by the age of the whole plant. The hypothesis that enrichment of the foliage with nitrogen and potassium may enhance host resistance to Alternaria and thus reduce disease severity, was examined for potato and tomato (A. solani ) and for cotton (A. macrospora ). Under controlled environment conditions, application of urea or KNO3 resulted in some reduction in disease development; however, foliar application of both nutrients (8-10 sprays in total) did not affect Alternaria severity in the field. Systemic fungicides against Alternaria (e.g. , tebuconazole and difenoconazole) are more effective than the commonly used protectant fungicides (e.g. mancozeb and chlorothalonil). Concepts for the integration of genotype resistance, age-related resistances and fungicide for the suppression of Alternaria diseases were developed and evaluated. It was found that reduction in host resistance, with age and among genotypes, can be compensated for by adjusting the intensity of fungicide applications, i.e. by increasing the frequency of sprays and by spraying systemic fungicides towards the end of the season. In, moderately resistant cultivars protection can be achieved by spraying at longer intervals than susceptible cultivars. The concepts for integration were evaluated in field trials for cotton, potatoes and tomatoes. By following these concepts it was possible to save up to five sprays out of 8-10 in a growing season.
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Freeman, Stanley, and Russell J. Rodriguez. The Interaction Between Nonpathogenic Mutants of Colletotrichum and Fusarium, and the Plant Host Defense System. United States Department of Agriculture, September 2000. http://dx.doi.org/10.32747/2000.7573069.bard.

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Анотація:
The intent of this proposal was to study the interaction between nonpathogenic mutants of Colletotrichum magna and Fusarium oxysporum, and the cucurbit host defense system. We had shown previously that a nonpathogenic endophytic mutant path- 1 of C. magna, caused no visible disease symptoms but protected watermelon seedlings from disease caused by the wildtype isolate and F. o. niveum. Objectives were: 1) Determine the microscopic, biochemical and molecular genetic interaction between "protected" (path- 1 colonized) cucurbit hosts and wildtype isolates of C. magna; 2) Isolate non-pathogenic mutants of F.o. melonis and test feasibility for protecting plants against fungal diseases. We found that path-1 caused no visible disease symptoms in cucurbit seedlings but conferred disease resistance against pathogenic isolates of C. magna, C. orbiculare, and F. oxysporum. Disease resistance conferred by path-1 correlated to a decrease in the time of activation of host defense systems after exposure of path-1 colonized plants to virulent pathogens. This was determined by monitoring the biochemical activity of PAL and peroxidase, and the deposition of lignin. It appears that path-1-conferred disease resistance is a multigenic phenomenon which should be more difficult for pathogen to overcome than single gene conferred resistance. Based on the benefits conferred by path-1, we have defined this mutant as expressing a mutualistic lifestyle. REMI (restriction enzyme-mediated integration) nonpathogenic mutants were also isolated using pHA1.3 plasmid linearized with Hind III and transformed into wildtype C. magna. The integrated vector and flanking genomic DNA sequences in REMI mutant R1 was re-isolated and cloned resulting in a product of approximately 11 kb designated pGMR1. Transformations of wildtype C. magna with pGMR1 resulted in the same non-pathogenic phenotype. A nonpathogenic mutant of F.o. melonis (pathogenic to melon) was isolated that colonized melon plants but elicited no disease symptoms in seedlings and conferred 25 - 50% disease protection against the virulent wildtype isolate. Subsequently, nonpathogenic mutant isolates of F.o. niveum (pathogenic to watermelon) were also isolated. Their protection capacity against the respective wildtype parent is currently under investigation. This research has provided information toward a better understanding of host-parasite interactions; specifically, endophytes, pathogens and their hosts. It will also allow us to assess the potential for utilizing nonpathogenic mutants as biological control agents against fungal pathogens and isolating molecular genetic factors of pathogenicity in Fusarium.
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4

Rodriguez, Russell, and Stanley Freeman. Characterization of fungal symbiotic lifestyle expression in Colletotrichum and generating non-pathogenic mutants that confer disease resistance, drought tolerance, and growth enhancement to plant hosts. United States Department of Agriculture, February 2005. http://dx.doi.org/10.32747/2005.7587215.bard.

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Анотація:
Fungal plant pathogens are responsible for extensive annual crop and revenue losses throughout the world. To better understand why fungi cause diseases, we performed gene-disruption mutagenesis on several pathogenic Colletotrichum species and demonstrated that pathogenic isolates can be converted to symbionts (mutualism, commensalism, parasitism) expressing non-pathogenic lifestyles. The objectives of this proposal were to: 1- generate crop-specific mutants by gene disruption that express mutualistic lifestyles, 2- assess the ability of the mutualists to confer disease resistance, drought tolerance, and growth enhancement to host plants, 3- compare fslm1 sequences and their genomic locations in the different species, and 4- document the colonization process of each Colletotrichum species.It was demonstrated that wildtype pathogenic Colletotrichum isolates, can be converted by mutation from expressing a pathogenic lifestyle to symbionts expressing non-pathogenic lifestyles. In the US, mutants of Colletotrichum were isolated by homologous gene disruption using a vector containing a disrupted FSlm1 sequence while in Israel, C. acutatum mutants were selected by restriction enzyme mediated integration (REMI) transformation. One group (US) of non-pathogenic mutants conferred disease protection against pathogenic species of Colletotrichum, Fusarium, and Phytophthora; drought tolerance; and growth enhancement to host plants. These mutants were defined as mutualists and disease resistance correlated to a decrease in the time required for hosts to activate defense systems when exposed to virulent fungi. The second group (Israel) of non-pathogenic mutants did not confer disease resistance and were classified as commensals. In addition, we demonstrated that wildtype pathogenic Colletotrichum species can express non-pathogenic lifestyles, including mutualism, on plants they colonize asymptomatically. The expected long term contribution of this research to agriculture in the US and Israel is threefold. Host-specific mutualists will be utilized in the various crops to confer (1) disease resistance to reduce dependence on chemical fungicides; (2) drought tolerance to reduce water consumption for irrigation; (3) growth enhancement to increase yields.
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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.

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Анотація:
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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6

Rodriguez, Russell J., and Stanley Freeman. Gene Expression Patterns in Plants Colonized with Pathogenic and Non-pathogenic Gene Disruption Mutants of Colletotrichum. United States Department of Agriculture, February 2009. http://dx.doi.org/10.32747/2009.7592112.bard.

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Анотація:
Fungal plant pathogens are responsible for extensive annual crop and revenue losses throughout the world. To better understand why fungi cause diseases, we performed gene-disruption mutagenesis on several pathogenic Colletotrichum species and demonstrated that pathogenic isolates can be converted to symbionts expressing non-pathogenic lifestyles. One group of nonpathogenic mutants confer disease protection against pathogenic species of Col!etotrichum, Fusarium and Phytophthora; drought tolerance; and growth enhancement to host plants. These mutants have been defined as mutualists and disease resistance correlates to a decrease in the time required for hosts to activate defense systems when exposed to virulent fungi. A second group of non-pathogenic mutants did not confer disease resistance and were classified as commensals. In addition, we have demonstrated that wildtype pathogenic Colletotrichum species can express non-pathogenic lifestyles, including mutualism, on plants they colonize asymptomatically. We have been using wildtype and isogenic gene disruption mutants to characterize gene expression patterns in plants colonized with a pathogen, mutualist or commensal. The US group is contrasting genes expressed during colonization by mutuahstic and commensal mutants of C. magna and a pathogenic wildtype C. coccodes on tomato. The Israeli group is characterizing genes expressed during asymptomatic colonization of tomato by wildtype C. acutatum and a non-pathogenic mutant.To accomplish this we have been utilizing suppressive subtraction hybridization, microarray and sequencing strategies. The expected contribution of this research to agriculture in the US and Israel is: 1) understanding how pathogens colonize certain hosts asymptomatic ally will shed light on the ecology of plant pathogens which has been described as a fundamental deficiency in plant pathology; 2) identifying genes involved in symbiotically conferred disease resistance will help explain why and how pathogens cause disease, and may identify new candidate targets for developing genetically modified disease resistant crop plants.
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7

Dickman, Martin B., and Oded Yarden. Characterization of the chorismate mutase effector (SsCm1) from Sclerotinia sclerotiorum. United States Department of Agriculture, January 2015. http://dx.doi.org/10.32747/2015.7600027.bard.

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Анотація:
Sclerotinia sclerotiorum is a filamentous fungus (mold) that causes plant disease. It has an extremely wide range of hosts (>400 species) and causes considerable damage (annual multimillion dollar losses) in economically important crops. It has proven difficult to control (culturally or chemically) and host resistance to this fungus has generally been inadequate. It is believed that this fungus occurs in almost every country. Virulence of this aggressive pathogen is bolstered by a wide array of plant cell wall degrading enzymes and various compounds (secondary metabolites) produced by the fungus. It is well established that plant pathogenic fungi secrete proteins and small molecules that interact with host cells and play a critical role in disease development. Such secreted proteins have been collectively designated as “effectors”. Plant resistance against some pathogens can be mediated by recognition of such effectors. Alternatively, effectors can interfere with plant defense. Some such effectors are recognized by the host plant and can culminate in a programmed cell death (PCD) resistant response. During the course of this study, we analyzed an effector in Sclerotiniasclerotiorum. This specific effector, SsCM1 is the protein chorismatemutase, which is an enzyme involved in a pathway which is important in the production of important amino acids, such a Tryptophan. We have characterized the Sclerotiniaeffector, SsCM1, and have shown that inactivation of Sscm1 does not affect fungal vegetative growth, development or production of oxalic acid (one of this fungus’ secondary metabolites associated with disease) production. However, yhis does result in reduced fungal virulence. We show that, unexpectedly, the SsCM1 protein translocates to the host chloroplast, and demonstrated that this process is required for full fungal virulence. We have also determined that the fungal SsCM1 protein can interact with similar proteins produced by the host. In addition, we have shown that the fungal SsCM1 is able to suppress at least some of the effects imposed by reactive oxygen species which are produced as a defense mechanism by the host. Last, but not least, the results of our studies have provided evidence contradicting the current dogma on at least some of the mechanist aspects of how this pathogen infects the host. Contrary to previousons, indicating that this pathogen kills its host by use of metabolites and enzymes that degrade the host tissue (a process called necrotrophy), we now know that at least in the early phases of infection, the fungus interacts with live host tissue (a phenomenon known as biotrophy). Taken together, the results of our studies provide novel insights concerning the mechanistic aspects of Sclerotinia-host interactions. We hope this information will be used to interfere with the disease cycle in a manner that will protect plants from this devastating fungus.
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8

Mawassi, Munir, Adib Rowhani, Deborah A. Golino, Avichai Perl, and Edna Tanne. Rugose Wood Disease of Grapevine, Etiology and Virus Resistance in Transgenic Vines. United States Department of Agriculture, November 2003. http://dx.doi.org/10.32747/2003.7586477.bard.

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Анотація:
Rugose wood is a complex disease of grapevines, which occurs in all growing areas. The disease is spread in the field by vector transmission (mealybugs). At least five elongated-phloem- limited viruses are implicated in the various rugose wood disorders. The most fully characterized of these are Grapevine virus A (GV A) and GVB, members of a newly established genus, the vitivirus. GVC, a putative vitivirus, is much less well characterized than GV A or GVB. The information regarding the role of GVC in the etiology and epidemiology of rugose wood is fragmentary and no sequence data for GVC are available. The proposed research is aimed to study the etiology and epidemiology of rugose wood disease, and to construct genetically engineered virus-resistant grapevines. The objectives of our proposed research were to construct transgenic plants with coat protein gene sequences designed to induce post-transcriptional gene silencing (pTGS); to study the epidemiology and etiology of rugose wood disease by cloning and sequencing of GVC; and surveying of rugose wood- associated viruses in Californian and Israeli vineyards. In an attempt to experimentally define the role of the various genes of GV A, we utilized the infectious clone, inserted mutations in every ORF, and studied the effect on viral replication, gene expression, symptoms and viral movement. We explored the production of viral RNAs in a GV A-infected Nicotiana benthamiana herbaceous host, and characterized one nested set of three 5'-terminal sgRNAs of 5.1, 5.5 and 6.0 kb, and another, of three 3'-terminal sgRNAs of 2.2, 1.8 and 1.0 kb that could serve for expression of ORFs 2-3, respectively. Several GV A constructs have been assembled into pCAMBIA 230 I, a binary vector which is used for Angrobacterium mediated transformation: GV A CP gene; two copies of the GV A CP gene arranged in the same antisense orientation; two copies of the GV A CP gene in which the downstream copy is in an antigens orientation; GV A replicase gene; GV A replicase gene plus the 3' UTR sequence; and the full genome of GV A. Experiments for transformation of N. benthamiana and grapevine cell suspension with these constructs have been initiated. Transgenic N. benthamiana plants that contained the CP gene, the replicase gene and the entire genome of GV A were obtained. For grapevine transformation, we have developed efficient protocols for transformation and successfully grapevine plantlets that contained the CP gene and the replicase genes of GV A were obtained. These plants are still under examination for expression of the trans genes. The construction of transgenic plants with GV A sequences will provide, in the long run, a means to control one of the most prevalent viruses associated with grapevines. Our many attempts to produce a cDNA library from the genome of GVC failed. For surveying of rugose wood associated viruses in California vineyards, samples were collected from different grape growing areas and tested by RT-PCR for GV A, GVB and GVD. The results indicated that some of the samples were infected with multiple viruses, but overall, we found higher incidence of GVB and GV A infection in California vineyards and new introduction varieties, respectively. In this research we also conducted studies to increase our understanding of virus - induced rootstock decline and its importance in vineyard productivity. Our results provided supporting evidence that the rootstock response to virus infection depends on the rootstock genotype and the virus type. In general, rootstocks are differ widely in virus susceptibility. Our data indicated that a virus type or its combination with other viruses was responsible in virus-induced rootstock decline. As the results showed, the growth of the rootstocks were severely affected when the combination of more than one virus was present.
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9

Sniezko, Richard A., Alvin D. Yanchuk, John T. Kliejunas, Katharine M. Palmieri, Janice M. Alexander, and Susan J. Frankel. Proceedings of the fourth international workshop on the genetics of host-parasite interactions in forestry: Disease and insect resistance in forest trees. Albany, CA: U.S. Department of Agriculture, Forest Service, Pacific Southwest Research Station, 2012. http://dx.doi.org/10.2737/psw-gtr-240.

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10

Wisniewski, Michael E., Samir Droby, John L. Norelli, Noa Sela, and Elena Levin. Genetic and transcriptomic analysis of postharvest decay resistance in Malus sieversii and the characterization of pathogenicity effectors in Penicillium expansum. United States Department of Agriculture, January 2014. http://dx.doi.org/10.32747/2014.7600013.bard.

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Анотація:
Blue mold of apple caused by Penicilliumexpansumis a major postharvest disease. Selection for postharvest disease resistance in breeding programs has been ignored in favor of fruit quality traits such as size, color, taste, etc. The identification of postharvest disease resistance as a heritable trait would represent a significant accomplishment and has not been attempted in apple. Furthermore, insight into the biology of the pathogenicity of P. expansumin apple could provide new approaches to postharvest decay management. Hypothesis: Postharvest resistance of apple to P. expansumcan be mapped to specific genetic loci and significant quantitative-trait-loci (QTLs) can be identified that account for a major portion of the population variance. Susceptibility of apple fruit to P. expansumis dependent on the ability of the pathogen to produce LysM effectors that actively suppress primary and/or secondary resistance mechanisms in the fruit. Objectives: 1) Identify QTL(s) and molecular markers for blue mold resistance in GMAL4593 mapping population (‘Royal Gala’ X MalussieversiiPI613981), 2) Characterize the transcriptome of the host and pathogen (P. expansum) during the infection process 3) Determine the function of LysM genes in pathogenicity of P. expansum. Methods: A phenotypic evaluation of blue mold resistance in the GMAL4593 mapping population, conducted in several different years, will be used for QTL analysis (using MapQTL 6.0) to identify loci associated with blue mold resistance. Molecular markers will be developed for the resistance loci. Transcriptomic analysis by RNA-seq will be used to conduct a time course study of gene expression in resistant and susceptible apple GMAL4593 genotypes in response to P. expansum, as well as fungal responses to both genotypes. Candidate resistance genes identified in the transcriptomic study and or bioinformatic analysis will be positioned in the ‘Golden Delicious’ genome to identify markers that co-locate with the identified QTL(s). A functional analysis of LysM genes on pathogenicity will be conducted by eliminating or reducing the expression of individual effectors by heterologous recombination and silencing technologies. LysMeffector genes will also be expressed in a yeast expression system to study protein function. Expected Results: Identification of postharvest disease resistance QTLs and tightly-linked genetic markers. Increased knowledge of the role of effectors in blue mold pathogenic
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