RESUMEN
BACKGROUND: Quinoa (Chenopodium quinoa Willd.) is an ancient grain crop that is tolerant to abiotic stress and has favorable nutritional properties. Downy mildew is the main disease of quinoa and is caused by infections of the biotrophic oomycete Peronospora variabilis Gaüm. Since the disease causes major yield losses, identifying sources of downy mildew tolerance in genetic resources and understanding its genetic basis are important goals in quinoa breeding. RESULTS: We infected 132 South American genotypes, three Danish cultivars and the weedy relative C. album with a single isolate of P. variabilis under greenhouse conditions and observed a large variation in disease traits like severity of infection, which ranged from 5 to 83%. Linear mixed models revealed a significant effect of genotypes on disease traits with high heritabilities (0.72 to 0.81). Factors like altitude at site of origin or seed saponin content did not correlate with mildew tolerance, but stomatal width was weakly correlated with severity of infection. Despite the strong genotypic effects on mildew tolerance, genome-wide association mapping with 88 genotypes failed to identify significant marker-trait associations indicating a polygenic architecture of mildew tolerance. CONCLUSIONS: The strong genetic effects on mildew tolerance allow to identify genetic resources, which are valuable sources of resistance in future quinoa breeding.
Asunto(s)
Chenopodium quinoa/genética , Chenopodium quinoa/microbiología , Variación Genética , Peronospora/patogenicidad , Enfermedades de las Plantas/microbiología , Chenopodium album/microbiología , Genoma de Planta , Estudio de Asociación del Genoma Completo , Genotipo , Interacciones Huésped-Patógeno/genética , Modelos Lineales , Peronospora/aislamiento & purificación , Enfermedades de las Plantas/etiología , Enfermedades de las Plantas/genética , Saponinas/análisis , Semillas/química , América del Sur , Secuenciación Completa del GenomaRESUMEN
Downy mildew is widespread throughout the world. However, the damage that it causes has not been studied in Brazil yet. The objective of this work was to evaluate which components of soybean yield are affected by downy mildew and to determine the coefficient of damage. Two field experiments were conducted in Castro (2006/07) and Ponta Grossa (2007/08) in the state of Parana, Brazil. The experimental design consisted of completely randomized blocks of (i) six treatments and five replications for the 2006/07 and (ii) eight treatments and four replications for the 2007/08 field experiments. Potassium phosphite (750g a.i. ha-1), propamocarb + fenamidone (900g a.i. ha-1) and mancozeb (2400g a.i. ha-1) were applied. In all of the treatments, the maximum severity of downy mildew infection occurred at growth stage R5.3, and the percentage of severity ranged between 0 and 43%. The disease gradient was obtained only on the second season. Equations of damage were generated for the yield and grain weight. The number of grains per pod and the number of pods per plant were not affected by downy mildew but, the weight of 1000 seeds per plant was reduced linearly with increasing of mildew severity.(AU)
O míldio da soja é disseminado em todo mundo. Entretanto, o dano que ele causa não tem sido estudado no Brasil. O objetivo deste trabalho foi avaliar quais componentes de rendimento da soja são afetados por essa doença e determinar o coeficiente de dano. Dois experimentos foram conduzidos, um em Castro (2006/07) e outro em Ponta Grossa (2007/08), no Estado do Paraná, Brasil. O delineamento experimental foi de blocos ao acaso com (i) seis tratamentos e cinco repetições para os experimentos de campo, safras 2006/07, e (ii) oito tratamentos e quatro repetições para 2007/08. Foram aplicados fosfito de potássio (750g ia ha-1), propamocarb + fenamidona (900g ia ha-1) e mancozeb (2,400g ia ha-1). Em todos os tratamentos, a severidade máxima da infecção pelo míldio ocorreu no estádio R5.3 e a porcentagem de severidade variou entre 0 e 43%. O gradiente da doença foi obtido apenas na segunda safra. Equações de danos foram geradas para o peso de grãos e produtividade. O número de grãos por vagem e o número de vagens por planta não foram afetados pelo míldio mas o peso de 1000 sementes por planta foi reduzido linearmente com o aumento da severidade do míldio.(AU)
Asunto(s)
Enfermedades de las Plantas , Glycine max/crecimiento & desarrollo , Glycine max/parasitología , Peronospora/patogenicidadRESUMEN
Blue mould [Peronospora hyoscyami f. sp. tabacina (Adam) Skalicky 1964] is one of the most important foliar diseases of tobacco that causes significant losses in the Americas, south-eastern Europe and the Middle East. This review summarizes the current knowledge of the mechanisms employed by this oomycete pathogen to colonize its host, with emphasis on molecular aspects of pathogenicity. In addition, key biochemical and molecular mechanisms involved in tobacco resistance to blue mould are discussed. TAXONOMY: Kingdom: Chromista (Straminipila); Phylum: Heterokontophyta; Class: Oomycete; Order: Peronosporales; Family: Peronosporaceae; Genus: Peronospora; Species: Peronospora hyoscyami f. sp. tabacina. DISEASE SYMPTOMS: The pathogen typically causes localized lesions on tobacco leaves that appear as single, or groups of, yellow spots that often coalesce to form light-brown necrotic areas. Some of the leaves exhibit grey to bluish downy mould on their lower surfaces. Diseased leaves can become twisted, such that the lower surfaces turn upwards. In such cases, the bluish colour of the diseased plants becomes quite conspicuous, especially under moist conditions when sporulation is abundant. Hence the name of the disease: tobacco blue mould. INFECTION PROCESS: The pathogen develops haustoria within plant cells that are thought to establish the transfer of nutrients from the host cell, and may also act in the delivery of effector proteins during infection. RESISTANCE: Several defence responses have been reported to occur in the Nicotiana tabacum-P. hyoscyami f. sp. tabacina interaction. These include the induction of pathogenesis-related genes, and a correlated increase in the activities of typical pathogenesis-related proteins, such as peroxidases, chitinases, beta-1,3-glucanases and lipoxygenases. Systemic acquired resistance is one of the best characterized tobacco defence responses activated on pathogen infection.