scholarly journals Effect of Air and Growing Medium Temperatures on Rhizoctonia Foot Rot of Epipremnum aureum

1990 ◽  
Vol 8 (3) ◽  
pp. 139-141
Author(s):  
A.R. Chase ◽  
R.T. Poole
Keyword(s):  
Rhizoctonia Solani ◽  
Fungal Pathogen ◽  
Disease Development ◽  
Foot Rot ◽  
Growth Reduction ◽  
Growing Medium ◽  
Epipremnum Aureum ◽  
Significant Disease ◽  
Continuous Temperature

Abstract Air and growing medium temperatures affected severity of foot rot of Epipremnum aureum (pothos) caused by Rhizoctonia solani AG4. Maximum daily temperatures of 30°C (86°F) for either air or soil resulted in optimal disease development. Maximum daily temperatures of 35°C (95°F) decreased disease development significantly due to fungal pathogen growth reduction. A continuous temperature of 30°C (86°F) was also too high for significant disease development.

Highly polymorphic microsatellite loci in the rice- and maize-infecting fungal pathogen Rhizoctonia solani anastomosis group 1 IA

2008 ◽  
Vol 8 (3) ◽  
pp. 686-689 ◽  
Author(s):  
M. ZALA ◽  
B. A. MCDONALD ◽  
J. BERNARDES DE ASSIS ◽  
M. B. CIAMPI ◽  
M. STORARI ◽  
...  
Keyword(s):  
Rhizoctonia Solani ◽  
Microsatellite Loci ◽  
Fungal Pathogen ◽  
Anastomosis Group ◽  
Polymorphic Microsatellite ◽  
Group 1

Characteristics of a disease of Sphagnum fuscum caused by Scleroconidioma sphagnicola

2001 ◽  
Vol 79 (10) ◽  
pp. 1217-1224 ◽  
Author(s):  
A Tsuneda ◽  
M H Chen ◽  
R S Currah
Keyword(s):  
Cell Wall ◽  
Fungal Pathogen ◽  
Infected Leaf ◽  
Disease Development ◽  
Cortical Cells ◽  
Necrotrophic Pathogen ◽  
Sphagnum Fuscum ◽  
Entire Plant ◽  
Host Cell Wall ◽  
Advanced Stages

Scleroconidioma sphagnicola Tsuneda, Currah & Thormann, a dematiaceous hyphomycetous fungus, was found to cause a disease of Sphagnum fuscum (Schimp.) Klinggr. Hyphae of S. sphagnicola penetrated into chlorophyllose cells of host leaves and caused degeneration of chloroplasts, resulting in chlorosis of the infected leaves. Parasite hyphae often grew inside the host cell wall, and cavities were created around the hyphae. The invaded cell wall of Sp. fuscum appeared swollen and showed wavy deformation. In advanced stages of disease development, infected leaf chlorophyllose cells and stem cortical cells were necrotic and the entire plant became brown, shriveled, and brittle. Hyphae of S. sphagnicola began to form microsclerotia during early stages of disease development. Microsclerotia either formed conidiogenous cells on their surface or remained metabolically inactive and did not form conidiogenous cells. It was concluded that S. sphagnicola is a necrotrophic pathogen of Sp. fuscum, and its morphological and phenological features show remarkable adaptations for dispersal and colonization as a pathogen in bog habitats.Key words: moss, fungal pathogen, pathogenesis, chlorosis, necrosis, microsclerotia.

Anthracnose of Florida Beggarweed (Desmodium tortuosum) Caused byColletotrichum truncatum

Weed Science ◽  
1988 ◽  
Vol 36 (3) ◽  
pp. 329-334 ◽  
Author(s):  
John Gardina ◽  
Robert H. Littrell ◽  
Richard T. Hanlin
Keyword(s):  
Relative Humidity ◽  
Host Specificity ◽  
Plant Species ◽  
Fungal Pathogen ◽  
Disease Development ◽  
Colletotrichum Truncatum ◽  
Optimum Conditions ◽  
Cotyledon Stage ◽  
Chamber Studies ◽  
Growth Chamber Studies

Greenhouse and growth chamber studies were conducted to determine conditions for infection of the fungal pathogenColletotrichum truncatum(Schw.) Andrus and Moore on Florida beggarweed (Desmodium tortuosum(Sw.) DC. # DEDTO and to determine the host specificity of this fungus. Optimum conditions for disease development were 14 to 16 h incubation in 100% relative humidity (RH) at 24 to 29 C. Control of Florida beggarweed with 105to 107C. truncatumspores/ml was greatest in the cotyledon stage and decreased with plant age. Ten of 18Desmodiumspecies tested were susceptible to the Florida beggarweed isolate ofC. truncatumbut 13 other plant species and varieties were resistant and 61 were immune.

scholarly journals Proteomic and genetic approaches to identifying defence-related proteins in rice challenged with the fungal pathogen Rhizoctonia solani

2006 ◽  
Vol 7 (5) ◽  
pp. 405-416 ◽  
Author(s):  
JOOHYUN LEE ◽  
TERRY M. BRICKER ◽  
MICHAEL LEFEVRE ◽  
SHANNON R. M. PINSON ◽  
JAMES H. OARD
Keyword(s):  
Rhizoctonia Solani ◽  
Fungal Pathogen ◽  
Related Proteins

Host Gamma Aminobutyric Acid Metabolic Pathway is involved in Resistance against Rhizoctonia solani

2020 ◽  
Author(s):  
Mamta Rani ◽  
Gopaljee Jha
Keyword(s):  
Gene Silencing ◽  
Rhizoctonia Solani ◽  
Fungal Pathogen ◽  
Large Scale ◽  
Aminobutyric Acid ◽  
Primary Metabolism ◽  
Succinic Semialdehyde ◽  
Gamma Aminobutyric Acid ◽  
Succinic Semialdehyde Dehydrogenase ◽  
Semialdehyde Dehydrogenase

Rhizoctonia solani is a highly destructive necrotrophic fungal pathogen having a diverse host range, including rice and tomato. Previously R. solani infection in rice has been found to cause large-scale readjustment in host primary metabolism and accumulation of various stress associated metabolites such as gamma aminobutyric acid (GABA). In this study, we report upregulation of GABA shunt genes during pathogenesis of R. solani in rice as well as tomato. The exogenous application of GABA provided partial resistance against R. solani infection in both the hosts. Further, using virus induced gene silencing (VIGS) approach, we knocked down the expression of some of the tomato genes involved in GABA biosynthesis (glutamate decarboxylase; GAD) and GABA catabolism (GABA-transaminase; GABA-T and succinic semialdehyde dehydrogenase; SSADH) to study their role in host defense against R. solani infection. The silencing of each of these genes was found to enhance disease susceptibility in tomato. Overall the results from gene expression analysis, exogenous chemical treatment and gene silencing studies suggest that GABA pathway plays a positive role in plant resistance against necrotrophic fungal pathogen R. solani.

scholarly journals Cutinase and Other Lipolytic Esterases Protect Bean Leaves from Infection by Rhizoctonia solani

1998 ◽  
Vol 11 (6) ◽  
pp. 514-522 ◽  
Author(s):  
Diana M. Parker ◽  
Wolfram Köller
Keyword(s):  
Rhizoctonia Solani ◽  
Esterase Activity ◽  
Venturia Inaequalis ◽  
Protective Mechanism ◽  
Disease Development ◽  
Mechanical Wounding ◽  
Small Areas ◽  
Pathogenesis Related ◽  
Web Blight ◽  
Bean Leaves

The results describe a novel activity of fungal cutinase, the protection of bean leaves from disease. Development of web blight symptoms on bean leaves infected with Rhizoctonia solani (AG-1) was prevented in the presence of cutinase purified from Venturia inaequalis. Instead of disease, small areas of tissue necrosis became visible, and the tissue in which the pathogen was restricted displayed strong autofluorescence beneath the inoculation sites. Mechanical wounding of the leaf surface had no effect on disease development and the permeability of the cuticle was not increased by cutinase action, indicating that surface wounding was not the cause for this novel activity of cutinase. A comparative study involving cutinase and other serine hydrolases revealed that the disease prevention resided in the lipolytic esterase activity rather than the cutinase activity. The pattern of expression of four pathogenesis-related (PR) protein genes provided no evidence for the modulation of known resistance responses of bean leaves in response to cutinase action. The protective mechanism of the esterase activity remains unknown.

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