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P A Roberts - One of the best experts on this subject based on the ideXlab platform.
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a fusarium Wilt resistance gene in gossypium barbadense and its effect on root knot nematode Wilt disease complex
Phytopathology, 2006Co-Authors: C Wang, P A RobertsAbstract:Wang, C., and Roberts, P. A. 2006. A Fusarium Wilt resistance gene in Gossypium barbadense and its effect on root-knot nematode-Wilt disease complex. Phytopathology 96:727-734. Fusarium Wilt, caused by the soilborne pathogen Fusarium oxysporum f. sp. vasinfectum race 1, is a vascular disease in cotton (Gossypium spp.), and is a component of a disease complex with root-knot nematodes (Meloidogyne incognita). Genetic analysis of two interspecific crosses (G. barbadense Pima S-7 × G. hirsutum Acala NemX and Pima S-7 × Acala SJ-2) showed that one major gene (designated Fov1 ) with allele dosage effect conferred resistance to F. oxysporum f. sp. vasinfectum race 1 in Pima S-7. Two amplified fragment length polymorphism (AFLP) markers were linked to Fov1 in Pima S-7, with genetic distance from the gene of 9.3 and 14.6 centimorgans. Less severe Wilt symptoms in Acala NemX than Acala SJ-2 indicated that Acala NemX possesses one or more minor genes contributing to delay of Wilt symptoms. Highly resistant plants in F2 and F3 (Pima S-7 × NemX) families indicated transgressive segregation effects of minor genes in Acala NemX combined with Fov1 from Pima S-7. The effects of Wilt and nematode resistance on the nematode–Wilt disease complex were assayed with two inoculation methods. In the presence of both pathogens, Wilt damage measured as shoot and root weight reductions was greatest on Wilt- and nematode-susceptible Acala SJ-2 and least in root-knot nematode-resistant and Wilt-susceptible Acala NemX. Intermediate damage occurred in Wilt-resistant and root-knot nematode-susceptible Pima S-7. The results indicated that nematode resistance was more effective than Wilt resistance in suppressing Wilt symptoms when either resistance was present alone. Nematode resistance combined with intermediate Wilt resistance, as in the F1 (Pima S-7 × NemX), was highly effective in protecting plants from root-knot nematodes and race 1 of Fusarium Wilt as a disease complex.
M Duffy - One of the best experts on this subject based on the ideXlab platform.
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feasibility of delaying removal of row covers to suppress bacterial Wilt of muskmelon cucumis melo
Plant Disease, 2011Co-Authors: Saalau E Rojas, Mark L Gleason, Jean C Batzer, M DuffyAbstract:Bacterial Wilt, caused by Erwinia tracheiphila, is a major disease of cucurbit crops in the United States. Management of the disease relies on controlling two vector species, striped (Acalymma vittatum) and spotted (Diabrotica undecimpunctata) cucumber beetles. Six field trials were conducted at Iowa State University research farms during 2007, 2008, and 2009 to assess the efficacy of delayed removal of spunbond polypropylene row covers to control bacterial Wilt on muskmelon (Cucumis melo). Treatments were (i) row cover removed at anthesis (conventional timing of removal), (ii) covers removed 10 days after row cover ends were opened at anthesis, (iii) covers removed 10 days after bumble bee hives were inserted under row covers at anthesis, and (iv) a noncovered control. In two field trials during 2007 and 2008, the delayed-removal row-cover treatments significantly suppressed bacterial Wilt throughout the growing season and enhanced yield compared with the noncovered and removal-at-anthesis controls. In Gilbert in 2008, however, bacterial Wilt suppression was equivalent among all three row-cover treatments. No bacterial Wilt was observed during three trials in 2009, and there was minimal difference in marketable yield among treatments. Net returns were compared using partial budget and sensitivity analyses. Melon prices and occurrence of bacterial Wilt had a strong impact on net returns. Using row covers increased production costs by 45%. In site years in which bacterial Wilt occurred, delaying removal of row covers resulted in the highest returns. When bacterial Wilt was absent, however, the delayed-removal row-cover treatments had the lowest returns. Results of the sensitivity analysis indicated that delaying removal of row covers for 10 days could be a cost-effective component of an integrated bacterial Wilt suppression strategy for muskmelon where bacterial Wilt occurs ≥50% of production seasons.
S. L. Brown - One of the best experts on this subject based on the ideXlab platform.
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Epidemiology and management of tomato spotted Wilt in peanut
Annual review of phytopathology, 2003Co-Authors: Albert K. Culbreath, J. W. Todd, S. L. BrownAbstract:■ Abstract Tomato spotted Wilt caused by thrips-vectored tomato spotted Wilt virus (TSWV) is a very serious problem in peanut (Arachis hypogaea L.) production. TSWV and the thrips Frankliniella fusca and Frankliniella occidentalis, which vector the virus, present a difficult and complicated challenge from the perspectives of both epidemiology and disease management. Simply controlling the vector typically has not resulted in control of spotted Wilt. No single measure can currently provide adequate control of spotted Wilt where severe epidemics occur. However, interdisciplinary investigations have resulted in development of integrated management systems that make use of moderately resistant cultivars and chemical and cultural practices, each of which helps to suppress spotted Wilt epidemics. Such systems have been successfully deployed in many areas for minimizing losses to this disease. The development of a spotted Wilt risk index has aided greatly in relaying information on the importance of using an integrated approach for managing this disease.
Jean C Batzer - One of the best experts on this subject based on the ideXlab platform.
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Bacterial Wilt of Cucurbits: Resurrecting a Classic Pathosystem
Plant disease, 2015Co-Authors: Erika Saalau Rojas, Jean C Batzer, Gwyn A. Beattie, Shelby J. Fleischer, Lori R. Shapiro, Mark A. Williams, Ricardo Bessin, Benny D. Bruton, T. Jude Boucher, Laura C.h. JesseAbstract:Bacterial Wilt threatens cucurbit crop production in the Midwestern and Northeastern United States. The pathogen, Erwinia tracheiphila, is a xylem-limited bacterium that affects most commercially important cucurbit species, including muskmelon, cucumber, and squash. Bacterial Wilt is transmitted and overwintered by striped and spotted cucumber beetles. Since there are few commercially available resistant cultivars, disease management usually relies on use of insecticides to suppress vector populations. Although bacterial Wilt was initially described more than 100 years ago, our knowledge of disease ecology and epidemiology advanced slowly for most of the 20th century. However, a recent wave of research has begun to fill in missing pieces of the bacterial Wilt puzzle. This article-the first review of research toward understanding the cucurbit bacterial Wilt pathosystem-recounts early findings and updates our understanding of the disease cycle, including pathogen and vector biology. We also highlight research areas that could lead to more efficient and ecologically based management of bacterial Wilt.
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feasibility of delaying removal of row covers to suppress bacterial Wilt of muskmelon cucumis melo
Plant Disease, 2011Co-Authors: Saalau E Rojas, Mark L Gleason, Jean C Batzer, M DuffyAbstract:Bacterial Wilt, caused by Erwinia tracheiphila, is a major disease of cucurbit crops in the United States. Management of the disease relies on controlling two vector species, striped (Acalymma vittatum) and spotted (Diabrotica undecimpunctata) cucumber beetles. Six field trials were conducted at Iowa State University research farms during 2007, 2008, and 2009 to assess the efficacy of delayed removal of spunbond polypropylene row covers to control bacterial Wilt on muskmelon (Cucumis melo). Treatments were (i) row cover removed at anthesis (conventional timing of removal), (ii) covers removed 10 days after row cover ends were opened at anthesis, (iii) covers removed 10 days after bumble bee hives were inserted under row covers at anthesis, and (iv) a noncovered control. In two field trials during 2007 and 2008, the delayed-removal row-cover treatments significantly suppressed bacterial Wilt throughout the growing season and enhanced yield compared with the noncovered and removal-at-anthesis controls. In Gilbert in 2008, however, bacterial Wilt suppression was equivalent among all three row-cover treatments. No bacterial Wilt was observed during three trials in 2009, and there was minimal difference in marketable yield among treatments. Net returns were compared using partial budget and sensitivity analyses. Melon prices and occurrence of bacterial Wilt had a strong impact on net returns. Using row covers increased production costs by 45%. In site years in which bacterial Wilt occurred, delaying removal of row covers resulted in the highest returns. When bacterial Wilt was absent, however, the delayed-removal row-cover treatments had the lowest returns. Results of the sensitivity analysis indicated that delaying removal of row covers for 10 days could be a cost-effective component of an integrated bacterial Wilt suppression strategy for muskmelon where bacterial Wilt occurs ≥50% of production seasons.
C Wang - One of the best experts on this subject based on the ideXlab platform.
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a fusarium Wilt resistance gene in gossypium barbadense and its effect on root knot nematode Wilt disease complex
Phytopathology, 2006Co-Authors: C Wang, P A RobertsAbstract:Wang, C., and Roberts, P. A. 2006. A Fusarium Wilt resistance gene in Gossypium barbadense and its effect on root-knot nematode-Wilt disease complex. Phytopathology 96:727-734. Fusarium Wilt, caused by the soilborne pathogen Fusarium oxysporum f. sp. vasinfectum race 1, is a vascular disease in cotton (Gossypium spp.), and is a component of a disease complex with root-knot nematodes (Meloidogyne incognita). Genetic analysis of two interspecific crosses (G. barbadense Pima S-7 × G. hirsutum Acala NemX and Pima S-7 × Acala SJ-2) showed that one major gene (designated Fov1 ) with allele dosage effect conferred resistance to F. oxysporum f. sp. vasinfectum race 1 in Pima S-7. Two amplified fragment length polymorphism (AFLP) markers were linked to Fov1 in Pima S-7, with genetic distance from the gene of 9.3 and 14.6 centimorgans. Less severe Wilt symptoms in Acala NemX than Acala SJ-2 indicated that Acala NemX possesses one or more minor genes contributing to delay of Wilt symptoms. Highly resistant plants in F2 and F3 (Pima S-7 × NemX) families indicated transgressive segregation effects of minor genes in Acala NemX combined with Fov1 from Pima S-7. The effects of Wilt and nematode resistance on the nematode–Wilt disease complex were assayed with two inoculation methods. In the presence of both pathogens, Wilt damage measured as shoot and root weight reductions was greatest on Wilt- and nematode-susceptible Acala SJ-2 and least in root-knot nematode-resistant and Wilt-susceptible Acala NemX. Intermediate damage occurred in Wilt-resistant and root-knot nematode-susceptible Pima S-7. The results indicated that nematode resistance was more effective than Wilt resistance in suppressing Wilt symptoms when either resistance was present alone. Nematode resistance combined with intermediate Wilt resistance, as in the F1 (Pima S-7 × NemX), was highly effective in protecting plants from root-knot nematodes and race 1 of Fusarium Wilt as a disease complex.
