Magnaporthe grisea

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Magnaporthe grisea
Conidium and conidiogenous cell
Scientific classification Edit this classification
Domain: Eukaryota
Kingdom: Fungi
Division: Ascomycota
Class: Sordariomycetes
Order: Magnaporthales
Family: Magnaporthaceae
Genus: Magnaporthe
Species:
M. grisea
Binomial name
Magnaporthe grisea
(T.T. Hebert) M.E. Barr
Synonyms

Ceratosphaeria grisea T.T. Hebert, (1971)
Dactylaria grisea (Cooke) Shirai, (1910)
Dactylaria oryzae (Cavara) Sawada, (1917)
Magnaporthe oryzae
Phragmoporthe grisea (T.T. Hebert) M. Monod, (1983)
Pyricularia grisea Sacc., (1880) (anamorph)
Pyricularia grisea (Cooke) Sacc., (1880)
Pyricularia oryzae Cavara, (1891)
Trichothecium griseum Cooke,
Trichothecium griseum Speg., (1882)

Magnaporthe grisea, also known as rice blast fungus, rice rotten neck, rice seedling blight, blast of rice, oval leaf spot of graminea, pitting disease, ryegrass blast, Johnson spot,

cryptic species complex containing at least two biological species that have clear genetic differences and do not interbreed.[14] Complex members isolated from Digitaria have been more narrowly defined as M. grisea. The remaining members of the complex isolated from rice and a variety of other hosts have been renamed Magnaporthe oryzae, within the same M. grisea complex.[14]
Confusion on which of these two names to use for the rice blast pathogen remains, as both are now used by different authors.

Members of the M. grisea complex can also infect other agriculturally important

Hosts and symptoms

Differential of lesions on rice leaves
Differential on rice

M. grisea is an

plant pathogen as it can reproduce both sexually and asexually to produce specialized infectious structures, appressoria, that infect aerial tissues and hyphae that can infect root
tissues.

Rice blast has been observed on rice strains M-201, M-202, M-204, M-205, M-103, M-104, S-102, L-204, Calmochi-101, with M-201 being the most vulnerable.[16] Initial symptoms are white to gray-green lesions or spots with darker borders produced on all parts of the shoot, while older lesions are elliptical or spindle-shaped and whitish to gray with necrotic borders. Lesions may enlarge and coalesce to kill the entire leaf. Symptoms are observed on all above-ground parts of the plant.[17] Lesions can be seen on the leaf collar, culm, culm nodes, and panicle neck node. Internodal infection of the culm occurs in a banded pattern. Nodal infection causes the culm to break at the infected node (rotten neck).[18] It also affects reproduction by causing the host to produce fewer seeds. This is caused by the disease preventing maturation of the actual grain.[15]

Disease cycle

Spores

The pathogen infects as a spore that produces lesions or spots on parts of the rice plant such as the leaf, leaf collar, panicle, culm and culm nodes. Using a structure called an

conidiospores.[20] After overwintering in sources such as rice straw and stubble, the cycle repeats.[15]

A single cycle can be completed in about a week under favorable conditions where one lesion can generate up to thousands of spores in a single night. Disease lesions, however, can appear in three to four days after infection.[21] With the ability to continue to produce the spores for over 20 days, rice blast lesions can be devastating to susceptible rice crops.[22]

Infection of

resistance against this pathogen.[23]

Environment

Rice blast is a significant problem in temperate regions and can be found in areas such as irrigated lowland and upland.

Sporulation increases with high relative humidity and at 25–28 °C (77–82 °F), spore germination, lesion formation, and sporulation are at optimum levels.[15]

In terms of control, excessive use of

drought stress increase rice susceptibility to the pathogen as the plant is placed in a weakened state and its defenses are low.[15] Flooding and draining fields is normal in rice growing, however leaving a field drained for extended periods also favors infection as that will aerate the soil, converting ammonium to nitrate and thus causing stress to rice crops, as well.[15]

Geographical distribution

Wheat blast was found in the 2017-2018 rainy season in Zambia, in the Mpika district of the Muchinga Province.[25][26]

In February 2016 a devastating wheat epidemic struck Bangladesh.[27][28] Transcriptome analysis showed this to be an M. grisea lineage most likely from Minas Gerais, São Paulo, Brasília, and Goiás states of Brazil and not from any geographically proximate strains.[27][28] This successful diagnosis shows the ability of genetic surveillance to untangle the novel biosecurity implications of transcontinental transportation[27][28] and allows the Brazilian experience to be rapidly applied to the Bangladeshi situation.[27][28] To that end the government has set up an early warning system to track its spread through the country.[28]

Management

J. Sendra rice

This fungus faces both

Rosmarinus officinalis to be effective in vitro, and provides treatment thresholds.[30]
: 107–108 

The wheat blast strain can be diagnosed by sequencing.

: 45 

Some innovative biologically-imitative fungicides are being developed from

Importance

Rice blast is the most important disease concerning rice crops in the world. Since rice is an important food source for much of the world, its effects have a broad range. It has been found in over 85 countries across the world and reached the United States in 1996. Every year the amount of crops lost to rice blast could feed 60 million people. Although there are some resistant strains of rice, the disease persists wherever rice is grown. The disease has never been eradicated from a region.[32]

Strains

Three strains, albino (defined by a mutation at the ALB1 locus), buff (BUF1), and rosy (RSY1) have been extensively studied because they are nonpathogenic. This has been found to be due to nonuse of melanin, which is a virulence factor in M. grisea.[1]: 184  The pathovar triticum strain (M. o. pv. triticum) causes the wheat blast disease.[12]

Genetics

Whole-genome sequences were just becoming possible, and being made available, in 2003.[13]

A

pmk1 is genetically close to one necessary for mating and cell morphology in yeasts, FUS3/KSS1. Defective mutant yeast are somewhat or entirely restored in mating function if they are given a copy of pmk1. It was therefore assumed that this must only be a mating and development gene in M. grisea, however it turns out to be both vital to the female mating process and in appressorium function and pathogenicity as a whole.[13]

Because signal links between MAPKs and

Ustilago maydis and several others, this was assumed to be true for M. grisea, and yet that was then shown to be unnecessary in this model. This demonstrates significant variety in cellular function within fungi.[13]

The transaminase alanine: glyoxylate aminotransferase 1 (AGT1) has been shown to be crucial to the pathogenicity of M. grisea through its maintenance of redox homeostasis in peroxisomes. Lipids transported to the appressoria during host penetration are degraded within a large central vacuole, a process that produces fatty acids. β-Oxidation of fatty acids is an energy producing process that generates Acetyl-CoA and the reduced molecules FADH2 and NADH, which must be oxidized in order to maintain redox homeostasis in appressoria. AGT1 promotes lactate fermentation, oxidizing NADH/FADH2 in the process.[33]

M. grisea mutants lacking the AGT1 gene were observed to be nonpathogenic through their inability to penetrate host surface membranes. This indicates the possibility of impaired lipid utilization in M. grisea appressoria in the absence of the AGT1 gene.[34]

Biochemistry of host-pathogen interactions

A 2010 review reported

PthXo2.[38]

See also

References

  1. ^
    PMID 14527276
    . Three mutants of M. grisea, albino, buff, and rosy (corresponding to the ALB1, BUF1, and RSY1 loci, respectively), have been studied extensively and are nonpathogenic. This is due to an inability to cross the plant cuticle because of the lack of melanin deposition in the appressorium.
  2. Centre for Agriculture and Bioscience International
    .
  3. .
  4. .
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  7. ^ Magnaporthe grisea Archived 2007-10-12 at the Wayback Machine at Crop Protection Compendium Archived 2007-07-16 at the Wayback Machine, CAB International
  8. ISSN 1935-9411
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  13. ^ .
  14. ^ .
  15. ^ on 2006-09-11. Retrieved 2014-02-25.
  16. University of California Integrated Pest Management
    (UC-IPM)
  17. ^ Rice Blast at the Online Information Service for Non-Chemical Pest Management in the Tropics
  18. ^ Rice Blast Archived 2010-10-20 at the Wayback Machine at Factsheets on Chemical and Biological Warfare Agents
  19. PMID 29567712
    .
  20. Elsevier Academic Press
    .
  21. .
  22. ^ Diagnostic Methods for Rice Blast[permanent dead link] at PaDIL Plant Biosecurity Toolbox
  23. ^ a b Liu, Xinyu; Zhang, Zhengguang (2022). "A double-edged sword: reactive oxygen species (ROS) during the rice blast fungus and host interaction". The FEBS Journal. 289 (18).
    S2CID 237340135
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  24. ^ a b Kuyek, Devlin (2000). "Implications of corporate strategies on rice research in asia". Grain. Retrieved 2010-10-20.
  25. ^ "Researchers in Zambia confirm: Wheat blast has made the intercontinental jump to Africa". 24 September 2020. Archived from the original on 6 October 2021. Retrieved 1 October 2020.
  26. S2CID 221843315
    .
  27. ^ .
  28. ^ a b c d e "New infographic highlights an early warning system for wheat blast in Bangladesh". CGIAR WHEAT. 2020-07-15. Archived from the original on 2020-12-01. Retrieved 2020-12-26.
  29. ^ Kurahasi, Yoshio (1997). "Biological Activity of Carpropamid (KTU 3616): A new fungicide for rice blast disease". Journal of Pesticide Science. Retrieved 2014-02-25.
  30. S2CID 199492358
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  31. ^ .
  32. ^ Rice Blast Archived 2010-07-31 at the Wayback Machine at Cereal Knowledge Bank
  33. PMID 22558413
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  34. .
  35. .
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  37. ^ .
  38. .

Further reading

External links