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Important Foliar Disease (important + foliar_disease)

Distribution by Scientific Domains

Life Sciences	75%

Selected Abstracts

Molecular mapping of the leaf rust resistance gene Rph7 in barley

PLANT BREEDING, Issue 5 2000
A. Graner
Abstract Leaf rust of barley, caused by Puccinia hordei Otth, is an important foliar disease in most temperate regions of the world. Sixteen major leaf rust resistance (Rph) genes have been described from barley, but only a few have been mapped. The leaf rust resistance gene Rph7 was first described from the cultivar ,Cebada Capa' and has proven effective in Europe. Previously mapped restriction fragment length polymorphism (RFLP) markers have been used to determine the precise location of this gene in the barley genome. From the genetic analysis of a ,Bow-man'/,Cebada Capa' cross, Rph7 was mapped to the end of chromosome 3HS, 1.3 recombination units distal to the RFLP marker cMWG691. A codominant cleaved amplified polymorphic site (CAPS) marker was developed by exploiting allele-specific sequence information of the cMWG691 site and adjacent fragments of genomic DNA. Based on the large amount of polymorphism present in this region, the CAPS marker may be useful for the marker-assisted selection of Rph7 in most diverse genetic backgrounds. [source]

Inhibition of photosynthesis and modification of the wheat leaf proteome by Ptr ToxB: A host-specific toxin from the fungal pathogen Pyrenophora tritici-repentis

PROTEINS: STRUCTURE, FUNCTION AND BIOINFORMATICS, Issue 16 2010
Yong Min Kim
Abstract Tan spot, caused by Pyrenophora tritici-repentis, is an important foliar disease of wheat. The fungus produces the host-specific, chlorosis-inducing toxin Ptr ToxB. To better understand toxin action, we examined the effects of Ptr ToxB on sensitive wheat. Photosynthesis, as measured by infrared gas analysis, declined significantly within 12,h of toxin treatment, prior to the development of chlorosis at 48,72,h. Analysis by 2-DE revealed a total of 102 protein spots with significantly altered intensities 12,36,h after toxin treatment, of which 66 were more abundant and 36 were less abundant than in the buffer-treated control. The identities of 47 of these spots were established by MS/MS, and included proteins involved in the light reactions of photosynthesis, the Calvin cycle, and the stress/defense response. Based on the declines in photosynthesis and the identities of the differentially abundant proteins, we hypothesize that Ptr ToxB causes a rapid disruption in the photosynthetic processes of sensitive wheat, leading to the generation of ROS and oxidative stress. Although the photoprotective and repair mechanisms of the host appear to initially still be functional, they are probably overwhelmed by the continued production of ROS, leading to chlorophyll photooxidation and the development of chlorosis. [source]

Suppression of southern corn leaf blight by a plant growth-promoting rhizobacterium Bacillus cereus C1L

ANNALS OF APPLIED BIOLOGY, Issue 1 2010
Chien-Jui Huang
Southern corn leaf blight (SCLB) is an important foliar disease of maize. In this study, an induced systemic resistance (ISR)-eliciting rhizobacterium Bacillus cereus C1L was used to protect maize against SCLB. Application of B. cereus C1L in maize rhizosphere effectively protected maize from SCLB under greenhouse and field conditions. The protection effect of B. cereus C1L was similar to that of Maneb (2 kg active ingredient per hectare), a recommended fungicide. Furthermore, possible factors of B. cereus C1L to elicit ISR and to promote plant growth were investigated. The results indicate that secreted factors and rhizosphere colonisation ability of B. cereus C1L are involved in ISR elicitation. In addition to biocontrol activity, B. cereus C1L was able to promote growth of maize in field. Compared with a non-treated control, leaf length, leaf width, plant height and fresh and dry weights of B. cereus C1L-treated corn plants significantly increased. Therefore, B. cereus C1L acts as a plant growth-promoting rhizobacterium of maize. [source]

Tobacco blue mould disease caused by Peronospora hyoscyami f. sp. tabacina

MOLECULAR PLANT PATHOLOGY, Issue 1 2010
ORLANDO BORRÁS-HIDALGO
SUMMARY 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, ,-1,3-glucanases and lipoxygenases. Systemic acquired resistance is one of the best characterized tobacco defence responses activated on pathogen infection. [source]