| Magnaporthe grisea | |
|---|---|
 | |
| Conidium andconidiogenous cell | |
Scientific classification | |
| 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 griseaT.T. Hebert, (1971) | |
Magnaporthe grisea, also known asrice blast fungus,rice rotten neck,rice seedling blight, blast of rice,oval leaf spot of graminea,pitting disease,ryegrass blast,Johnson spot,[1][2][3][4][5][6][7]neck blast,[8][9][10][11]wheat blast[12] andImochi (稲熱), is a plant-pathogenicfungus andmodel organism[13] that causes a serious disease affectingrice. It is now known thatM. grisea consists of acryptic species complex containing at least two biological species that have clear genetic differences and do not interbreed.[14] Complex members isolated fromDigitaria have been more narrowly defined asM. grisea. The remaining members of the complex isolated from rice and a variety of other hosts have been renamedMagnaporthe oryzae, within the sameM. 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 theM. grisea complex can also infect other agriculturally importantcereals includingwheat,rye,barley, andpearl millet causing diseases calledblast disease orblight disease. Rice blast causes economically significant crop losses annually. Each year it is estimated to destroy enough rice to feed more than 60 million people. The fungus is known to occur in 85 countries worldwide[15] and as of 2003[update] was the most devastatingfungal plant pathogen in the world.[13]
M. grisea is anascomycete fungus. It is an extremely effectiveplant pathogen as it can reproduce both sexually and asexually to produce specialized infectious structures,appressoria, that infect aerial tissues and hyphae that can infectroot 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 theleaf collar,culm, culm nodes, andpanicle 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]
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 anappressorium, the pathogen penetrates the plant. The appressoriumcell wall ischitinous and its inner side containsmelanin.[1]: 184 which is necessary to damage host structures.[1]: 184 [13] Theturgor pressure generated during this process is sufficient to penetrate theplants' cuticles routinely, and experimentally can penetrateKevlar. This impressive turgor is produced by synthesis ofglycerol and maintained by the aforementioned appressorial melanin.[13] The pathogen is able to move between the plant cells using its invasive hyphae to enter throughplasmodesmata.[19]M. grisea then sporulates from the diseased rice tissue to be dispersed asconidiospores.[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 ofrice inducesphosphorylation of thelight-harvesting complex II protein LHCB5.[23] LHCB5 is required for areactive oxygen species burst produced by the host which providesresistance against this pathogen.[23]
Rice blast is a significant problem in temperate regions and can be found in areas such as irrigated lowland and upland.[24] Conditions conducive for rice blast include long periods of free moisture and/or high humidity, because leaf wetness is required for infection.[24]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 ofnitrogen fertilization as well asdrought stress increase ricesusceptibility 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, convertingammonium tonitrate and thus causing stress to rice crops, as well.[15]
Wheat blast was found in the 2017–2018 rainy season inZambia, in theMpika district of the Muchinga Province.[25][26]
In February 2016 a devastating wheat epidemic struckBangladesh.[27][28]Transcriptome analysis showed this to be anM. grisea lineage most likely fromMinas Gerais,São Paulo,Brasília, andGoiás states ofBrazil 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 thegovernment has set up an early warning system to track its spread through the country.[28]
This fungus faces bothfungicides andgenetic resistance in some types of rice developed byplant breeders. It is ableto establish bothresistance to those chemical treatments andvirulence tocrop resistance by genetic change through mutation. In order to most effectively control infection byM. grisea, an integrated management program should be implemented to avoid overuse of a single control method and fight against genetic resistance. For example, eliminating crop residue could reduce the occurrence of overwintering and discourage inoculation in subsequent seasons. Another strategy would be to plant resistant rice varieties that are not as susceptible to infection byM. grisea.[15] Knowledge of the pathogenicity ofM. grisea and its need for free moisture suggest other control strategies such as regulated irrigation and a combination of chemical treatments with different modes of action.[15] Managing the amount of water supplied to the crops limits spore mobility thus dampening the opportunity for infection. Chemical controls such asCarpropamid have been shown to prevent penetration of the appressoria into rice epidermal cells, leaving the grain unaffected.[29] Papajani et al. 2015 finds theessential oils of bothOriganum vulgare andRosmarinus officinalis to be effectivein vitro, and provides treatment thresholds.[30]: 107–108
The wheat blast strain can be diagnosed by sequencing.[12]: 45 Thierryet al., 2020 presents a set ofgenetic markers which can be found bypolymerase chain reaction (PCR),real-time PCR (RT-PCR), andloop-mediated isothermal amplification (LAMP).[12]: 45 The big advantages of the Thierry markers are that they do not missisolates lacking the Mot3 sequence, for exampleBR0032, and its greatsensitivity.[12]: 45
Some innovative biologically imitative fungicides are being developed fromsmall RNAs and shortpeptides.[31]SNP-D4 is a short peptide located by anin vitro library screen against theM. oryzaecalmodulin.[31] It binds to calmodulin, inhibitsconidia formation, and blocksspore germination.[31]
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]
Threestrains,albino (defined by a mutation at theALB1 locus),buff (BUF1), androsy (RSY1), have been extensively studied because they are nonpathogenic. This has been found to be due to their inability to synthesizemelanin, which is a virulence factor in some fungi.[1]: 184 Thepathovartriticum strain (M. o. pv.triticum) causes thewheat blast disease.[12] Export of Magnaporthe from the US is restricted.[33]
Whole-genome sequences were just becoming possible, and being made available, in 2003.[13]
Amitogen-activated protein kinase (MAPK) calledpmk1 is genetically close to one necessary formating andcell morphology inyeasts,FUS3/KSS1. Defective mutant yeast are somewhat or entirely restored in mating function if they are given a copy ofpmk1. It was therefore assumed that this must only be a mating and development gene inM. 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 andcyclic adenosine monophosphates were shown to be required for mating in several other models, includingUstilago maydis and several others, this was assumed to be true forM. grisea, and yet that was then shown to be unnecessary in this model. This demonstrates significant variety in cellular function within fungi.[13]
Thetransaminase alanine: glyoxylate aminotransferase 1 (AGT1) has been shown to be crucial to the pathogenicity ofM. 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 producesfatty acids.β-Oxidation of fatty acids is an energy producing process that generates Acetyl-CoA and the reduced moleculesFADH2 andNADH, which must be oxidized in order to maintain redox homeostasis in appressoria. AGT1 promotes lactate fermentation, oxidizing NADH/FADH2 in the process.[34]
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 inM. grisea appressoria in the absence of the AGT1 gene.[35]
A 2010 review reportedclones for quantitative disease resistance in plants.[36] The rice plant responds to the blast pathogen by releasingjasmonic acid, which cascades into the activation of further downstreammetabolic pathways which produce the defense response.[37] This accumulates as methyl-jasmonic acid.[37] The pathogen responds bysynthesizing anoxidizing enzyme which prevents this accumulation and its resulting alarm signal.[37]OsPii-2 is a rice protein that acts as animmunoreceptor.[38] It binds to the rice's ownExo70-F3protein.[38] This protein is a target of theM. oryzaeeffectorAVR-Pii that the fungus secretes during infection. Thus, this allows theOsPii-2 protein to monitor forM. oryzae's attack against that target.[38] Some rice cultivars carryresistance alleles of theOsSWEET13 gene, which produces the molecular target of theX. oryzae pv.oryzae effectorPthXo2.[39]
Three mutants ofM. grisea,albino,buff, androsy (corresponding to theALB1,BUF1, andRSY1 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.
