Magnaporthe grisea: Difference between revisions
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''M.grisea'' produces conidia spores that become airborne and so land on rice plants. The spores are adhesive and stick to the plant. Germination is then followed and a specialized structure called the appresorium penetrates the plant surface. High nitrogen content, host plant moisture, and 20°C of night temperatures favors the disease. There are many races of this fungal pathogen and their level of virulence varies. [[Rice cultivars]] have been bred with the different resistance genes that have been identified, however the pathogen overcomes the resistance genes within a few years. | ''M.grisea'' produces conidia spores that become airborne and so land on rice plants. The spores are adhesive and stick to the plant. Germination is then followed and a specialized structure called the appresorium penetrates the plant surface. High nitrogen content, host plant moisture, and 20°C of night temperatures favors the disease. There are many races of this fungal pathogen and their level of virulence varies. [[Rice cultivars]] have been bred with the different resistance genes that have been identified, however the pathogen overcomes the resistance genes within a few years. | ||
== | ==Control Measures== | ||
'''Burning/composting of diseased tissues''' | |||
Diseased plants are burned or composted to prevent the spread of the disease to the next crop season. | |||
'''Healthy Crop''' | |||
For a healthy crop, healthy seeds are necessary and many precautions are to be taken. The seeds are collected from the field where ''M.grisea'' existence is unlikely due to hostile conditions for the pathogen. Fungicide and disinfectants are then applied if necessary for protection against a variety of pathogens. | |||
'''Fertilizer management''' | |||
Excess nitrogen fertilizer can facilitate the disease progression, whereas silica limits the development of the disease. The amount and type of fertilizer are to be discretionally applied. | |||
'''Chemical control''' | |||
The following fungicides are applied to combat the rice blast disease: | |||
benomyl, fthalide, edifenphos, iprobenfos, tricyclazole, isoprothiolane, | |||
probenazole, pyroquilon, felimzone(= meferimzone), diclocymet, carpropamid, fenoxanil and metominostrobin, and antibiotics such as blasticidin and kasugamycin. | |||
'''Resistant cultivars''' | |||
Based on studies and current knowledge of the different races of ''M.grisea'', resistant cultivars have been bred throughout the world. | |||
==Current Research== | ==Current Research== | ||
==References== | ==References== |
Revision as of 08:36, 17 April 2009
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Magnaporthe grisea
A conidium and conidiogenous cell of M. grisea | ||||||||||||||
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Scientific classification | ||||||||||||||
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Binomial name | ||||||||||||||
Magnaporthe grisea |
Description and significance
Magnaporthe grisea, a plant-pathogenic fungus, is the causal agent of rice blast disease which is one of the greatest pathological threats to rice crops. It was thought to be localized only in developing nations, however for the past decade it has emerged as a severe problem in the United States, more recently in California. Yearly, rice that can feed an estimated 60 million people is destroyed by this disease. M.grisea is a well adapted fungus that can attack and penetrate its host plant with ease. More importantly, this fungus can also infect other important agricultures such as cereals, wheat, rye, pearl millet, and barley. The disease that is cause is then referred as blight disease or blast disease. Furthermore, M.grisea is thought of as a model organism in studies of fungal phytopathogenicity and host-parasite interactions.
Genome structure
Due to the destructive nature of this pathogen, sequencing the entire genome was necessary to understand the mechanisms of how the fungus causes disease. The complete genome of M.grisea was sequenced in 2005. M. grisea is a haploid and consists of ~40 Mb that are contained in 7 chromosomes (Talbot et al. 1993; Orbach 1996).The genome consists of a varied group of secreted proteins and a range of GPCR (G-Protein Coupled Receptors) genes. Furthermore, strong phylogenetic evidence of HGT’s (Horizontal Gene Transfer) has been found between M.grisea (ascomycete fungi) and oomycetes ( a distant relative).
Cell structure and metabolism
Magnaporthe grisea is a filamentous fungi. The spore tips contains a STM(Spore Tip Mucilage) adhesive that allows M.grisea to bind to its host. The binding of the spore begins the infection progression. After host-binding, specialized infection cells termed appresoria provide mechanical force and thus penetrates the plant cuticle and so gain entry into the internal tissues of the host.
M.grisea are infectious species and so obtain nutrients from their hosts. M.grisea is haploid and can reproduce sexually and asexually. M.grisea infectiious life cycle is asexual. The conidium is the infectious structure in this life cycle. After colonization of its host, lesions form. The lesions sites are locations of M.grisea sporulation. Soon enough, nearby plants become infected as well and so the spread of rice blast disease.
Ecology
M.grisea inhibits the host plant’s immune system, affecting the metabolism and cell signaling pathways. Adaptation of M.grisea is so efficient that even rice cultivars (bred to resist the disease) are infected. All above-ground parts of a host plant can be infected, but only if the stem, node, or panicle becomes infected will the grain set be lost. Rice is one of the most important staple food worldwide and control of this disease is utmost important.
Life Cycle
Pathology
M.grisea produces conidia spores that become airborne and so land on rice plants. The spores are adhesive and stick to the plant. Germination is then followed and a specialized structure called the appresorium penetrates the plant surface. High nitrogen content, host plant moisture, and 20°C of night temperatures favors the disease. There are many races of this fungal pathogen and their level of virulence varies. Rice cultivars have been bred with the different resistance genes that have been identified, however the pathogen overcomes the resistance genes within a few years.
Control Measures
Burning/composting of diseased tissues Diseased plants are burned or composted to prevent the spread of the disease to the next crop season.
Healthy Crop For a healthy crop, healthy seeds are necessary and many precautions are to be taken. The seeds are collected from the field where M.grisea existence is unlikely due to hostile conditions for the pathogen. Fungicide and disinfectants are then applied if necessary for protection against a variety of pathogens.
Fertilizer management Excess nitrogen fertilizer can facilitate the disease progression, whereas silica limits the development of the disease. The amount and type of fertilizer are to be discretionally applied.
Chemical control The following fungicides are applied to combat the rice blast disease: benomyl, fthalide, edifenphos, iprobenfos, tricyclazole, isoprothiolane, probenazole, pyroquilon, felimzone(= meferimzone), diclocymet, carpropamid, fenoxanil and metominostrobin, and antibiotics such as blasticidin and kasugamycin.
Resistant cultivars Based on studies and current knowledge of the different races of M.grisea, resistant cultivars have been bred throughout the world.