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Relevant bibliographies by topics / Host resistance

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Academic literature on the topic 'Host resistance'

Author: Grafiati

Published: 4 June 2021

Last updated: 20 February 2023

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Journal articles on the topic "Host resistance"

1

Van Loveren, H. "Host resistance models." Human & Experimental Toxicology 14, no. 1 (January 1995): 137–40. http://dx.doi.org/10.1177/096032719501400134.

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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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Pink, D. A. C., and P. Hand. "Plant resistance and strategies for breeding resistant varieties." Plant Protection Science 38, SI 1 - 6th Conf EFPP 2002 (January 1, 2002): S9—S14. http://dx.doi.org/10.17221/10310-pps.

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An explanation of the ‘boom-bust’ cycle of resistance breeding was provided by the gene-for-gene relationship between a pathogen and its host. Despite this understanding, most R genes continued to be deployed singly and resistance has been ephemeral. The reasons for breeding ‘single R gene’ varieties are discussed. Alternative strategies for the deployment of R genes and the use of quantitative race non-specific resistance have been advocated in order to obtain durable resistance. The feasibility of both of these approaches is discussed taking into account the impact of technologies such as plant transformation and marker-assisted selection. A change in focus from durability of the plant phenotype to that of the crop phenotype is advocated.

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ALLEN, J. R. "Host resistance to ectoparasites." Revue Scientifique et Technique de l'OIE 13, no. 4 (December 1, 1994): 1287–303. http://dx.doi.org/10.20506/rst.13.4.824.

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Yancey, Michael K. "HOST DEFENSES AND BACTERIAL RESISTANCE." Obstetrics and Gynecology Clinics of North America 19, no. 3 (September 1992): 413–34. http://dx.doi.org/10.1016/s0889-8545(21)00364-8.

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Loria, Roger M. "Neurosteroids and Host Immune Resistance." Advances in Neuroimmune Biology 5, no. 1 (2014): 33–42. http://dx.doi.org/10.3233/nib-140084.

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Buu, N., F. Sánchez, and E. Schurr. "The Bcg Host-Resistance Gene." Clinical Infectious Diseases 31, Supplement_3 (September 1, 2000): S81—S85. http://dx.doi.org/10.1086/314067.

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Burleson, Gary R., and Florence G. Burleson. "Influenza virus host resistance model." Methods 41, no. 1 (January 2007): 31–37. http://dx.doi.org/10.1016/j.ymeth.2006.09.007.

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Giga, D. P. "Host plant resistance to insects." Crop Protection 15, no. 5 (August 1996): 488–90. http://dx.doi.org/10.1016/0261-2194(96)84751-x.

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Ponpipom, Mitree M., William K. Hagmann, Laura A. O'Grady, Jesse J. Jackson, David D. Wood, and Hans J. Zweerink. "Glycolipids as host resistance stimulators." Journal of Medicinal Chemistry 33, no. 2 (February 1990): 861–67. http://dx.doi.org/10.1021/jm00164a062.

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Dissertations / Theses on the topic "Host resistance"

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Wilson, F. D., and H. M. Flint. "Host Plant Resistance." College of Agriculture, University of Arizona (Tucson, AZ), 1985. http://hdl.handle.net/10150/203923.

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Wilson, F. D., and H. M. Flint. "Host Plant Resistance." College of Agriculture, University of Arizona (Tucson, AZ), 1986. http://hdl.handle.net/10150/219754.

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The 1985 and 1986 Cotton Reports have the same publication and P-Series numbers.
Cotton breeding stocks were evaluated for resistance to pink bollworm. Resistance is being transferred into improved agronomic stocks.

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Fellowes, Mark Dominic Edmund. "Evolution of host resistance to parasitoid attack." Thesis, Imperial College London, 1998. http://hdl.handle.net/10044/1/8082.

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Sydorchuk, R. I. "Non-specific host resistance in acute trauma." Thesis, БДМУ, 2021. http://dspace.bsmu.edu.ua:8080/xmlui/handle/123456789/18659.

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Beswetherick, John T. "An ultrastructural study of host and non-host resistance reactions in plant cells." Thesis, Open University, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.292658.

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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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Chigurupati, Pavan Chandra. "Role of SABP2 in Tobacco Non-Host Resistance." Digital Commons @ East Tennessee State University, 2011. https://dc.etsu.edu/etd/1393.

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Plant innate immunity is activated upon pathogen attack by recognizing their avirulent (avr) genes by Resistant (R) genes leading to R-gene resistance or host resistance. Another form of innate immunity is non-host resistance that is exhibited by a given plant species to most strains of a microbial species. R-gene resistance activates salicylic acid (SA) that is synthesized from methyl salicylic acid (MeSA) by Salicylic Acid Binding Protein 2 (SABP2). It was hypothesized that SABP2 plays the similar role in non-host resistance also. Growth experiments and non-host related gene analysis experiments were conducted on tobacco plants using P.s tabaci and P.s. phaseolicola that are host and non-host pathogens on tobacco respectively. Tobacco control plant C3 that expresses SABP2 and 1-2 that is RNAi silenced in SABP2 expression were used in this study. Results suggest that SABP2 may not have any significant role in tobacco non-host resistance.

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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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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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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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Books on the topic "Host resistance"

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S, Khush Gurdev, ed. Host plant resistance to insects. Wallingford, Oxon, UK: CAB International in association with the International Rice Research Institute, 1995.

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

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

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

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Kumar Chakravarthy, Akshay, and Venkatesan Selvanarayanan, eds. Experimental Techniques in Host-Plant Resistance. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-2652-3.

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Kreier, Julius P. Infection, resistance and immunity. 2nd ed. New York, NY: Taylor & Francis, c2002., 2002.

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Kreier, Julius P. Infection, resistance and immunity. 2nd ed. New York, NY: Taylor & Francis, c2002., 2002.

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F, Mortensen Richard, ed. Infection, resistance, and immunity. New York: Harper & Row, 1990.

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9

Pande, S. Host plant resistance to Ascochyta blight of chickpea. Patancheru: International Crops Research Institute for the Semi-arid Tropics, 2010.

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

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Book chapters on the topic "Host resistance"

1

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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Shew, H. D., and B. B. Shew. "Host Resistance." In Epidemiology and Management of Root Diseases, 244–75. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-85063-9_8.

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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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Capinera, John L., Thomas O. Crist, John B. Heppner, Minos E. Tzanakakis, Severiano F. Gayubo, Aurélien Tartar, Pauline O. Lawrence, et al. "Host Plant Resistance." In Encyclopedia of Entomology, 1863. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6359-6_1408.

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Burleson, Stefanie C. M., Wendy Jo Freebern, Florence G. Burleson, Gary R. Burleson, Victor J. Johnson, and Robert W. Luebke. "Host Resistance Assays." In Methods in Molecular Biology, 117–45. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8549-4_9.

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Vohr, Hans-Werner, and Henk van Loveren. "Host Resistance Assays." In Encyclopedia of Immunotoxicology, 390–95. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-54596-2_691.

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Dent, David, and Richard H. Binks. "Host plant resistance." In Insect pest management, 103–50. Wallingford: CABI, 2020. http://dx.doi.org/10.1079/9781789241051.0103.

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Butter, N. S., and A. K. Dhawan. "Host Plant Resistance." In A Monograph on Whiteflies, 75–92. Boca Raton: CRC Press, 2021. http://dx.doi.org/10.1201/9781003095668-6.

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Mookiah, Shanthi, Banumathy Sivasubramaniam, Thiruveni Thangaraj, and Srinivasan Govindaraj. "Host Plant Resistance." In Molecular Approaches for Sustainable Insect Pest Management, 1–56. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-16-3591-5_1.

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Conference papers on the topic "Host resistance"

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Vosman, Ben. "Host plant resistance towards insects." In 2016 International Congress of Entomology. Entomological Society of America, 2016. http://dx.doi.org/10.1603/ice.2016.105645.

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Kaloshian, Isgouhi. "Aphid-host interactions: Effectors and resistance protein activation." In 2016 International Congress of Entomology. Entomological Society of America, 2016. http://dx.doi.org/10.1603/ice.2016.106255.

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Hodgson, Erin W., and Matt E. O'Neal. "Research update on host plant resistance for soybean aphid." In Proceedings of the 21st Annual Integrated Crop Management Conference. Iowa State University, Digital Press, 2010. http://dx.doi.org/10.31274/icm-180809-40.

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Nibouche, Samuel. "Genetic diversity inMelanaphis sacchariand host-plant resistance in sugarcane." In 2016 International Congress of Entomology. Entomological Society of America, 2016. http://dx.doi.org/10.1603/ice.2016.108360.

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"Effect of Sulfates in Concrete on Their Resistance to Freezing and Thawing." In "SP-177: Ettringite, the Sometimes Host of Destruction". American Concrete Institute, 1999. http://dx.doi.org/10.14359/6238.

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"Influence of C3 A Content of Cement on Frost and Scaling Resistance of Concrete." In "SP-177: Ettringite, the Sometimes Host of Destruction". American Concrete Institute, 1999. http://dx.doi.org/10.14359/6237.

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Prasifka, Jarrad. "Host plant resistance to sunflower insect pests in North America." In 2016 International Congress of Entomology. Entomological Society of America, 2016. http://dx.doi.org/10.1603/ice.2016.111207.

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Ismari, Dylan, and Jim Plusquellic. "IP-level implementation of a resistance-based physical unclonable function." In 2014 IEEE International Symposium on Hardware-Oriented Security and Trust (HOST). IEEE, 2014. http://dx.doi.org/10.1109/hst.2014.6855570.

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Arsath K F, Muhammad, Vinod Ganesan, Rahul Bodduna, and Chester Rebeiro. "PARAM: A Microprocessor Hardened for Power Side-Channel Attack Resistance." In 2020 IEEE International Symposium on Hardware Oriented Security and Trust (HOST). IEEE, 2020. http://dx.doi.org/10.1109/host45689.2020.9300263.

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"Effect of Infilling of Air Voids by Ettringite on Resistance of Concretes to Freezing and Thawing." In "SP-177: Ettringite, the Sometimes Host of Destruction". American Concrete Institute, 1999. http://dx.doi.org/10.14359/6239.

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Reports on the topic "Host resistance"

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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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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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Joel, Daniel M., Steven J. Knapp, and Yaakov Tadmor. Genomic Approaches for Understanding Virulence and Resistance in the Sunflower-Orobanche Host-Parasite Interaction. United States Department of Agriculture, August 2011. http://dx.doi.org/10.32747/2011.7592655.bard.

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Oroginal Objectives: (i) identify DNA markers linked to the avirulence (Avr) locus and locate the Avr locus through genetic mapping with an inter-race Orobanche cumana population; (ii) develop high-throughput fingerprint DNA markers for genotypingO. cumana races; (iii) identify nucleotide binding domain leucine rich repeat (NB-LRR) genes encoding R proteins conferring resistance to O. cumana in sunflower; (iv) increase the resolution of the chromosomal segment harboring Or₅ and related R genes through genetic and physical mapping in previously and newly developed mapping populations of sunflower; and (v) develop high-throughput DNA markers for rapidly and efficiently identifying and transferring sunflower R genes through marker-assisted selection. Revisions made during the course of project: Following changes in O. cumana race distribution in Israel, the newly arrived virulent race H was chosen for further analysis. HA412-HO, which was primarily chosen as a susceptible sunflower cultivar, was more resistant to the new parasite populations than var. Shemesh, thus we shifted sunflower research into analyzing the resistance of HA412-HO. We exceeded the deliverables for Objectives #3-5 by securing funding for complete physical and high-density genetic mapping of the sunflower genome, in addition to producing a complete draft sequence of the sunflower genome. We discovered limited diversity between the parents of the O. cumana population developed for the mapping study. Hence, the developed DNA marker resources were insufficient to support genetic map construction. This objective was beyond the scale and scope of the funding. This objective is challenging enough to be the entire focus of follow up studies. Background to the topic: O. cumana, an obligate parasitic weed, is one of the most economically important and damaging diseases of sunflower, causes significant yield losses in susceptible genotypes, and threatens production in Israel and many other countries. Breeding for resistance has been crucial for protecting sunflower from O. cumana, and problematic because new races of the pathogen continually emerge, necessitating discovery and deployment of new R genes. The process is challenging because of the uncertainty in identifying races in a genetically diverse parasite. Major conclusions, solutions, achievements: We developed a small collection of SSR markers for genetic mapping in O. cumana and completed a diversity study to lay the ground for objective #1. Because DNA sequencing and SNPgenotyping technology dramatically advanced during the course of the study, we recommend shifting future work to SNP discovery and mapping using array-based approaches, instead of SSR markers. We completed a pilot study using a 96-SNP array, but it was not large enough to support genetic mapping in O.cumana. The development of further SNPs was beyond the scope of the grant. However, the collection of SSR markers was ideal for genetic diversity analysis, which indicated that O. cumanapopulations in Israel considerably differ frompopulations in other Mediterranean countries. We supplied physical and genetic mapping resources for identifying R-genes in sunflower responsible for resistance to O. cumana. Several thousand mapped SNP markers and a complete draft of the sunflower genome sequence are powerful tools for identifying additional candidate genes and understanding the genomic architecture of O. cumana-resistanceanddisease-resistance genes. Implications: The OrobancheSSR markers have utility in sunflower breeding and genetics programs, as well as a tool for understanding the heterogeneity of races in the field and for geographically mapping of pathotypes.The segregating populations of both Orobanche and sunflower hybrids are now available for QTL analyses.

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Lapidot, Moshe, and Vitaly Citovsky. molecular mechanism for the Tomato yellow leaf curl virus resistance at the ty-5 locus. United States Department of Agriculture, January 2016. http://dx.doi.org/10.32747/2016.7604274.bard.

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Tomato yellow leaf curl virus (TYLCV) is a major pathogen of tomato that causes extensive crop loss worldwide, including the US and Israel. Genetic resistance in the host plant is considered highly effective in the defense against viral infection in the field. Thus, the best way to reduce yield losses due to TYLCV is by breeding tomatoes resistant or tolerant to the virus. To date, only six major TYLCV-resistance loci, termed Ty-1 to Ty-6, have been characterized and mapped to the tomato genome. Among tomato TYLCV-resistant lines containing these loci, we have identified a major recessive quantitative trait locus (QTL) that was mapped to chromosome 4 and designated ty-5. Recently, we identified the gene responsible for the TYLCV resistance at the ty-5 locus as the tomato homolog of the gene encoding messenger RNA surveillance factor Pelota (Pelo). A single amino acid change in the protein is responsible for the resistant phenotype. Pelo is known to participate in the ribosome-recycling phase of protein biosynthesis. Our hypothesis was that the resistant allele of Pelo is a “loss-of-function” mutant, and inhibits or slows-down ribosome recycling. This will negatively affect viral (as well as host-plant) protein synthesis, which may result in slower infection progression. Hence we have proposed the following research objectives: Aim 1: The effect of Pelota on translation of TYLCV proteins: The goal of this objective is to test the effect Pelota may or may not have upon translation of TYLCV proteins following infection of a resistant host. Aim 2: Identify and characterize Pelota cellular localization and interaction with TYLCV proteins: The goal of this objective is to characterize the cellular localization of both Pelota alleles, the TYLCV-resistant and the susceptible allele, to see whether this localization changes following TYLCV infection, and to find out which TYLCV protein interacts with Pelota. Our results demonstrate that upon TYLCV-infection the resistant allele of pelota has a negative effect on viral replication and RNA transcription. It is also shown that pelota interacts with the viral C1 protein, which is the only viral protein essential for TYLCV replication. Following subcellular localization of C1 and Pelota it was found that both protein localize to the same subcellular compartments. This research is innovative and potentially transformative because the role of Peloin plant virus resistance is novel, and understanding its mechanism will lay the foundation for designing new antiviral protection strategies that target translation of viral proteins. BARD Report - Project 4953 Page 2

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Sharon, Amir, and Tesfaye Mengiste. Molecular dissection of host and pathogen factors in Botrytis cinerea pathogenesis for improved genetic resistance. United States Department of Agriculture, January 2016. http://dx.doi.org/10.32747/2016.7604272.bard.

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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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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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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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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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Levin, Ilan, John Thomas, Moshe Lapidot, Desmond McGrath, and Denis Persley. Resistance to Tomato yellow leaf curl virus (TYLCV) in tomato: molecular mapping and introgression of resistance to Australian genotypes. United States Department of Agriculture, October 2010. http://dx.doi.org/10.32747/2010.7613888.bard.

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Tomato yellow leaf curl virus (TYLCV) is one of the most devastating viruses of cultivated tomatoes. Although first identified in the Mediterranean region, it is now distributed world-wide. Sequence analysis of the virus by the Australian group has shown that the virus is now present in Australia. Despite the importance of the disease and extensive research on the virus, very little is known about the resistance genes (loci) that determine host resistance and susceptibility to the virus. A symptom-less resistant line, TY-172, was developed at the Volcani Center which has shown the highest resistance level among all tested varieties. Preliminary results show that TY-172 is a good candidate to confer resistance to both TYLCV and to Tomato leaf curl virus (ToLCV) in Queensland conditions. Furthermore, Segregation analysis has previously indicated that the resistance is determined by 2-3 genes. In this proposal we aimed to substantiate that TY-172 can contribute to resistance breeding against TYLCV in Queensland, to develop DNA markers to advance such resistance breeding in both Israel and Queensland, and to exploit these markers for resistant breeding in Australian and Israeli lines. To map quantitative trait loci (QTLs) controlling TYLCVresistance in TY172, appropriate segregating populations were analyzed using 69 polymorphic DNA markers spanning the entire tomato genome. Results show that TYLCV resistance in TY172 is controlled by a previously unknown major QTL, originating from the resistant line, and four additional minor QTLs. The major QTL, termed Ty-5, maps to chromosome 4 and accounts for 39.7-to-46.6% of the variation in symptom severity among segregating plants (LOD score: 33-to-35). The minor QTLs, originated either from the resistant or susceptible parents, were mapped to chromosomes 1, 7, 9 and 11, and contributed 12% to the variation in symptom severity in addition to Ty-5. Further analysis of parental lines as well as large F₁, BC₁F₁, F₂ and BC₁F₂ populations originating from crosses carried out, in reciprocal manner, between TY172 and the susceptible processing line M-82 (LA3475) during spring-summer 2010, indicated that: (1) the minor QTLs we have previously identified are in effect not reproducible, (2)Ty-5 alone can yield highly resistant plants with practically no extra-chromosomal effects, and (3) the narrow-sense heritability estimate of resistance levels, attributed to additive factors responsive to selection, does not significantly deviate from 1. All of these results point to Ty-5 as the sole resistance locus in TY172 thus significantly increasing the likelihood of its successful molecular dissection. The DNA markers developed during the course of this study were transferred together with the TY172 genotype to Queensland. TY172 was crossed to a panel of Australian genotypes and the resulting populations were subjected to segregation analysis. Results showed that resistant locus, Ty-5, is highly reproducible in the Australian conditions as well. The Australian group was also able to make improvements to the marker assays by re-designing primer pairs to provide more robust PCR fragments. The Ty-5 locus has now been introgressed into elite Australian germplasm and selection for TYLCV resistance has begun. Cumulatively, our results show that Ty-5 can be effectively used, together with the TY172 genotype to expedite TYLCV resistance breeding and improve our understanding of the genetics that underline the response of tomato to TYLCV. Contributions to agriculture include: (1) the development of tools for more efficient resistance breeding, allowing the incorporation of resistance to local tomato varieties in Australia, Israel and elsewhere; and (2) establish a solid framework for a future attempt to clone the genes that encode such resistance. The latter will enable to decipher the resistance mechanisms that could be applied to other geminiviruses in tomato and possibly in other plant species.

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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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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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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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Grumet, Rebecca, and Benjamin Raccah. Identification of Potyviral Domains Controlling Systemic Infection, Host Range and Aphid Transmission. United States Department of Agriculture, July 2000. http://dx.doi.org/10.32747/2000.7695842.bard.

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Potyviruses form one of the largest and most economically important groups of plant viruses. Individual potyviruses and their isolates vary in symptom expression, host range, and ability to overcome host resistance genes. Understanding factors influencing these biological characteristics is of agricultural importance for epidemiology and deployment of resistance strategies. Cucurbit crops are subject to severe losses by several potyviruses including the highly aggressive and variable zucchini yellow mosaic virus (ZYMV). In this project we sought to investigate protein domains in ZYMV that influence systemic infection and host range. Particular emphasis was on coat protein (CP), because of known functions in both cell to cell and long distance movement, and helper component-protease (HC-Pro), which has been implicated to play a role in symptom development and long distance movement. These two genes are also essential for aphid mediated transmission, and domains that influence disease development may also influence transmissibility. The objectives of the approved BARD project were to test roles of specific domains in the CP and HC-Pro by making sequence alterations or switches between different isolates and viruses, and testing for infectivity, host range, and aphid transmissibility. These objectives were largely achieved as described below. Finally, we also initiated new research to identify host factors interacting with potyviral proteins and demonstrated interaction between the ZYMV RNA dependent RNA polymerase and host poly-(A)-binding protein (Wang et al., in press). The focus of the CP studies (MSU) was to investigate the role of the highly variable amino terminus (NT) in host range determination and systemic infection. Hybrid ZYMV infectious clones were produced by substituting the CP-NT of ZYMV with either the CP-NT from watermelon mosaic virus (overlapping, but broader host range) or tobacco etch virus (TEV) (non- overlapping host range) (Grumet et al., 2000; Ullah ct al., in prep). Although both hybrid viruses initially established systemic infection, indicating that even the non-cucurbit adapted TEV CP-NT could facilitate long distance transport in cucurbits, after approximately 4-6, the plants inoculated with the TEV-CPNT hybrid exhibited a distinct recovery of reduced symptoms, virus titer, and virus specific protection against secondary infection. These results suggest that the plant recognizes the presence of the TEV CP-NT, which has not been adapted to infection of cucurbits, and initiates defense responses. The CP-NT also appears to play a role in naturally occurring resistance conferred by the zym locus in the cucumber line 'Dina-1'. Patterns of virus accumulation indicated that expression of resistance is developmentally controlled and is due to a block in virus movement. Switches between the core and NT domains of ZYMV-NAA (does not cause veinal chlorosis on 'Dina-1'), and ZYMV-Ct (causes veinal chlorosis), indicated that the resistance response likely involves interaction with the CP-NT (Ullah and Grumet, submitted). At the Volcani Center the main thrust was to identify domains in the HC-Pro that affect symptom expression or aphid transmissibility. From the data reported in the first and second year report and in the attached publications (Peng et al. 1998; Kadouri et al. 1998; Raccah et al. 2000: it was shown that: 1. The mutation from PTK to PAK resulted in milder symptoms of the virus on squash, 2. Two mutations, PAK and ATK, resulted in total loss of helper activity, 3. It was established for the first time that the PTK domain is involved in binding of the HC-Pro to the potyvirus particle, and 4. Some of these experiments required greater amount of HC-Pro, therefore a simpler and more efficient purification method was developed based on Ni2+ resin.

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