User:Hannaheherring/Magnaporthe grisea

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Significance[edit]

Rice blast is one of the most devastating plant diseases that causes tremendous crop losses and ultimately threatens global food security. [1] Every year rice blast destroys between 10% to 30% of the annual rice harvest, or enough rice to feed 60 million people. [2] Considering rice composes 23% of the calories consumed worldwide, is the most important food product in Asia (home to 55% of the human population), where 93% of rice is grown, the importance of this issue is of understandable significance. [1] In addition to this, if the nutritional needs of the global population are to continue to be met, rice production will need to double over the next 40 years. [2] As such, research on the interaction between rice plants and the pathogen responsible for rice blast, M. oryzae, is crucial to understand both the pathogenicity of the fungus and the reciprocal plant immune response so these losses can begin to decrease.

Rice-Magnaporthe oryzae Pathosystem[edit]

M. oryzae vs M. grisea[edit]

It is important to clarify the difference between Magnaporthe oryzae and M. grisea, two closely related pathogens that are both commonly deemed responsible for rice blast disease. From research utilizing a multilocus genealogical approach, it was determined that M. oryzae arose as a novel species distinct from M. grisea.[3] These species, while morphologically indistinguishable, are separated into two clades based on their respective host species; M. grisea is associated with crabgrass (Digitaria), whereas M. oryzae is pathogenic to a variety of grasses and grains, the most notable being Oryza (rice).[1] [3] M. grisea is often cited as the pathogen responsible for rice blast, and while that is true for Digitaria, the fungus responsible for the infection of the rice crop are the rice-infecting strains of M. oryzae.[1]

Infection Mechanism[edit]

The infection of Oryza begins when a fungal spore lands on host leaves and immediately attaches by means of a specialized adherent.[4] This adhesive, released from the tip of the spore, bonds the germinating spore to the plant while it creates an appressorium, a cell designed to penetrate the host.[5] The appressorium generates phenomenal turgor pressure—up to 9 MPa—that creates the entry point for the pathogen after the leaf cuticle ruptures.[5] This occurs when the turgor is translated to mechanical force via formation of the penetration peg, a structure that forces its way through the cuticle and into the host epidermis.[6] Once the plant is breached, the hyphae of M. oryzae penetrate deeply into the tissue, creating the characteristic rice blast lesions.[1] The tissue is rapidly colonized, and photosynthesis is dramatically impacted.[7] In addition to entrance via appressorium on outer appendages of the plant, M. oryzae can infect using mechanisms characteristic of typical root-infecting pathogens.[8] By utilizing hyphopodia, a penetration structure, as well as a FOW1 (a mitochondrial carrier utilized in the wilt pathogen fungus Fusarium oxysporum) homologue, research has shown that M. oryzae can infect and spread from the roots to cause disease.[8]

M. oryzae is a hemibiotrophic pathogen, and therefore utilizes a mechanism that begins with an asymptomatic spread throughout the plant in a biotrophic phase, followed by a necrotrophic phase wherein host-cell death is induced.[9] Recent research has shown that the M. oryzae effector, AvrPiz-t, interacts with APIP5, (an Oryza bZIP transcription factor), by suppressing its transcriptional ability, a silencing that leads to cell death.[9] This process is regarded as effector-triggered necrosis, or ETN.[9] At the same time an NLR (nod-like receptor) protein in rice, Piz-t, acts to stabilize APIP5 and prevent necrosis, while APIP5 also acts reciprocally and stabilizes Piz-t. [9] Taken together, the research presents a budding model proposing how ETN can be suppressed in plants at the necrotrophic stage by an NLR receptor (a leucine-rich repeat encoded by the R protein for the purpose of detecting pathogen effector molecules), thus presenting a method of immunity to rice blast infection.

PTI: Pattern Triggered Immunity[edit]

Pattern triggered immunity (PTI) is one of two layers of defense plants have evolved to fight invading pathogens.[10] This first line of defense restricts pathogens by using surface-localized (plasma membrane) pattern-recognition receptors (PRRs) to recognize infecting pathogens and activate the immune system.[11] This system is thought to be an ancient form of plant innate immunity.[11][12]


The necrosis-inducing secreted protein 1 (NIS1) in M. oryzae targets host immune components that transmit signaling from PRRs.[10] NIS1 is regarded as a core effector (meaning it is conserved across a range of pathogens) and in M. oryzae, it has the ability to inhibit PTI signaling and suppress two defense responses; the hypersensitive response and oxidative burst.[10] In the event that M. oryzae lacks NIS1, research suggests a significant impairment of virulence on rice and barley, a finding that indicates the importance of the effector NIS1 for the infective ability of M. oryzae.[10]


Another important PRR in Oryza is CEBiP, a plasma membrane glycoprotein with a high affinity for chitin (a molecule common in vertebrates such as insects/crustaceans, as well as a component of the cell wall in fungi), that can recognize chitin particles and induce a defense.[13] This is made possible since chitin is not a naturally occurring molecule in plant systems, and as such, CEBiP is able to recognize the foreign material and enact defense mechanisms.


M. oryzae induces this response in Oryza in a variety of ways. To begin, the protein MSP1 plays an important role in the pathogenicity of the fungus.[14] Part of the cerato-platanin family (proteins capable of inducing disease-resistant responses via elicitor activity[15]), MSP1 is secreted by M. oryzae and triggers cell death in the host plant, as well as induces defense-related responses found in PTI.[14] The extent to which the presence of this molecule induces cell death points to its essential role in the resistance of M. oryzae in Oryza, since the occurrence of cell death indicates the plant immune responses fighting the pathogen. Similar to MSP1, the recently identified MoHrip1 is another secreted protein from M. oryzae that triggers PTI through its infection mechanisms.[16] Research indicates this protein plays a critical role in the fungal penetration and colonization of an infected host, and consequently is a trigger for the host plant to begin initiating defense mechanisms.[16] Current research suggests that further characterization of these fungal elicitors (and more information on precisely what functions they perform in the host plant) would be incredibly useful for furthering the understanding of M. Oryzae immune responses in Oryza.[14]

In terms of the initial breaching of the host plant, M. oryzae overcomes the first line of plant defense by secreting an effector protein termed, Secreted LysM protein, or Slp1.[17] This effector is able to bind to chitin to suppress the chitin-triggered immune responses, namely the CEBiP glycoprotein in Oryzae.[17] This mechanism functions by means of an accumulation of Slp1 between the rice plasma membrane and the fungal cell wall.[17] Like MSP1 and MoHrip1, Slp1 is a necessary component in the colonization of M. oryzae but differs in function by functioning in the tissue invasion role.[17] Another powerful effector protein that can inhibit rice immune responses is the previously discussed AvrPiz-t.[18] It is important to note that Slp1 and AvrPiz-t, while having a role in the virulence of M. oryzae like MSP1 and MoHrip1, also are triggers for plant immune responses. As such, this reciprocal interaction shows the co-evolotion of pathogens and plant defenses, as the presence of a pathogenic protein will cause a contrasting host defense.

ETI: Effector Triggered Immunity[edit]

After the initial immune response, the second layer of plant immunity is employed. This response is characterized by the utilization of polymorphic resistance (R) proteins in the host that become activated by the avirulence (Avr) effectors from the pathogen.[13] The effector triggered immunity (ETI) response is often associated with hypersensitive reactions and is well known to occur quickly and robustly.[13]

The R proteins are essential in this response, as they are one of the driving factors. Within the pathosystem, R proteins in Oryza either directly or indirectly recognize avirulence effectors to initiate a hypersensitive reaction that works to prevent pathogen infection.[9] These R-proteins are critical in fighting rice blast, as over 100 different R-genes have been identified as functioning in the resistance to M. oryzae.[19] Many of these R-genes encode proteins with a nucleotide binding site (NBS), coupled with a leucine rich repeat (LRR) domain.[20] These proteins are among the most amplified in plant families, widespread among many grass and grain species, and are important in recognizing and resisting pathogens.[20] In many cases, R effectors are paired singularly to an Avr effector, but in other cases, research has indicated two R proteins will act together to successfully inhibit the virulent effects of one Avr molecule.[19] Research has uncovered four atypical R genes found in rice that are not race specific like most, but rather exhibit differences in resistance mechanisms, such as unique motifs and novel epigenetic regulation.[19] The four genes are Pi21, Ptr, BSR-D1, and BSR-K1.[21] There are fifteen R proteins currently identified.[13] Although less thoroughly understood, Avr effectors are equally as important in the pathosystem and in the induction of the ETI response through the activating effects they induce in the host. There are currently nine Avr effectors characterized, as well as many other newly discovered molecules and effectors that assist in the defense and immunity from M. oryzea as they are recognized by R proteins.[13]

As a result of the recognition of PAMPS, (or pathogen associated molecular patterns, the molecules responsible for the induction of the initial PTI response) and Avr effectors, host plants defending themselves from fungal pathogens will initiate the hypersensitive response in the ETI stage of defense.[13] Research has indicated that most R-genes associated with rice blast are consequently also associated with a hypersensitive response, as proposed by the gene-for-gene concept and race specificity.[22] MoHrip1, mentioned above for its role in PTI, is responsible for the induction of the hypersensitive response (HR).[13] When M. oryzae infects a host and MoHrip1 is recognized by plant PRRs, the HR sets into motion cell death, which in turn triggers the cascade of associated host defenses such as H2O2 production, alkalization, and callose deposition.[13] While evidence suggests that MoHrip1 is involved in activating rice HR, further investigation is still required to confirm this point.[13]

Signaling Transduction & Downstream Responses[edit]

Rho (or rac) proteins are a small group of GTPases that serve as simple switches in a variety of signaling cascades.[13]  In the rice genome, seven Rac GTPases have been identified, and recent studies have illuminated their role in rice immunity.[13] One specific example of this is the OsRac1 protein, a GTPase that is induced by various PAMPS from M. oryzae (such as chitin) and participates in the PTI signaling in Oryza by propagating the signal.[13]  In addition to this, OsRac1 is also necessary in innate immunity functions mediated by the NBS-LRR protein Pit.[13] As such, it can be said that the OsRac protein is required for PTI and ETI responses in rice, an interesting but not surprising application of signaling cascade functions in plant immunity.

MAPK Signaling, CDPK Signaling, and Transcription Factors[edit]

Numerous studies have elucidated the importance of MAPK signaling in both PTI and ETI responses.[23] A notable MAPK gene from rice induced by M. oryzae infection is BWMK1, the first cloned MAPK gene that regulates the innate immune response for numerous different rice pathogens.[13]  In a similar way, CDPKs (calcium-dependent protein kinases) also generate downstream signaling responses in various plant processes, however, not much is currently understood about the role CDPKs play in rice immunity to pathogens.[13] Finally, transcription factors are also involved in the defenses against rice pathogens. Research indicates that there are many TF’s from a wide range of families (such as Ap2/Erf, bZIP, Zn-finger, NAC, MYB, WRKY, and others) that are involved in reactions to both biotic and abiotic stressors, and many TFs in the rice genome are utilized in innate immune responses.[24]

Future Directions[edit]

The Rice-M. oryzae pathosystem has provided significant insight into the plant immune system and has become the model interaction for demonstrating the impacts of fungal effectors and the consequential plant PTI/ETI responses. As previously stated, this pathoystem also demonstrates the co-evolution of a host and its pathogen. While M. Oryzae has evolved effectors capable of suppressing plant immune responses (such as Slp1 and AvrPiz-t), Oryza has consequently developed an innate immune system that can recognize these molecules and deploy PTI and ETI responses.[13] While there have been substantial gains made in the understanding of this pathogen and its interactions with its host, there are still many questions to be answered. These include (and are certainly not limited to), what are the functions of fungal effector targets that induce PTI, if there is an existence of cross-talk between PTI and ETI, and what occurs after R proteins become activated by recognizing Avr effectors.[13]

In addition to these molecular questions, it is critical that more research is invested into how fungal pathogens evade host defenses, how plant immunity can be strengthened, and how M. oryzae can ultimately be prevented in a crop so effective strategies for fighting rice blast can be developed, resistant cultivars can be created, and economic and environmental losses can be reduced.

References[edit]

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  2. ^ a b Skamnioti, Pari; Gurr, Sarah J. (2009-03-01). "Against the grain: safeguarding rice from rice blast disease". Trends in Biotechnology. 27 (3): 141–150. doi:10.1016/j.tibtech.2008.12.002. ISSN 0167-7799.
  3. ^ a b Couch, Brett C.; Kohn, Linda M. (2002-07-01). "A multilocus gene genealogy concordant with host preference indicates segregation of a new species, Magnaporthe oryzae, from M. grisea". Mycologia. 94 (4): 683–693. doi:10.1080/15572536.2003.11833196. ISSN 0027-5514. PMID 21156541.
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  14. ^ a b c Wang, Yiming; Wu, Jingni; Kim, Sang Gon; Tsuda, Kenichi; Gupta, Ravi; Park, Sook-Young; Kim, Sun Tae; Kang, Kyu Young (2016). "Magnaporthe oryzae-Secreted Protein MSP1 Induces Cell Death and Elicits Defense Responses in Rice". Molecular Plant-Microbe Interactions®. 29 (4): 299–312. doi:10.1094/mpmi-12-15-0266-r. ISSN 0894-0282.
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  16. ^ a b Nie, Hai-Zhen; Zhang, Lin; Zhuang, Hui-Qian; Shi, Wen-Jiong; Yang, Xiu-Fen; Qiu, De-Wen; Zeng, Hong-Mei (2019-04-02). "The Secreted Protein MoHrip1 Is Necessary for the Virulence of Magnaporthe oryzae". International Journal of Molecular Sciences. 20 (7): 1643. doi:10.3390/ijms20071643. ISSN 1422-0067.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  17. ^ a b c d Mentlak, Thomas A.; Kombrink, Anja; Shinya, Tomonori; Ryder, Lauren S.; Otomo, Ippei; Saitoh, Hiromasa; Terauchi, Ryohei; Nishizawa, Yoko; Shibuya, Naoto; Thomma, Bart P.H.J.; Talbot, Nicholas J. (2012-01-01). "Effector-Mediated Suppression of Chitin-Triggered Immunity by Magnaporthe oryzae Is Necessary for Rice Blast Disease". The Plant Cell. 24 (1): 322–335. doi:10.1105/tpc.111.092957. ISSN 1532-298X.
  18. ^ Skamnioti, Pari; Gurr, Sarah J. (2009). "Against the grain: safeguarding rice from rice blast disease". Trends in Biotechnology. 27 (3): 141–150. doi:10.1016/j.tibtech.2008.12.002. ISSN 0167-7799.
  19. ^ a b c Meng, Qingfeng; Gupta, Ravi; Min, Cheol Woo; Kwon, Soon Wook; Wang, Yiming; Je, Byoung Il; Kim, Yu-Jin; Jeon, Jong-Seong; Agrawal, Ganesh Kumar; Rakwal, Randeep; Kim, Sun Tae (2019-10-29). "Proteomics of Rice—Magnaporthe oryzae Interaction: What Have We Learned So Far?". Frontiers in Plant Science. 10. doi:10.3389/fpls.2019.01383. ISSN 1664-462X.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  20. ^ a b Yang, Sihai; Li, Jing; Zhang, Xiaohui; Zhang, Qijun; Huang, Ju; Chen, Jian-Qun; Hartl, Daniel L.; Tian, Dacheng (2013-10-21). "Rapidly evolving genes in diverse grass species confer resistance to rice blast disease". Proceedings of the National Academy of Sciences. 110 (46): 18572–18577. doi:10.1073/pnas.1318211110. ISSN 0027-8424.
  21. ^ Fukuoka, Shuichi; Saka, Norikuni; Koga, Hironori; Ono, Kazuko; Shimizu, Takehiko; Ebana, Kaworu; Hayashi, Nagao; Takahashi, Akira; Hirochika, Hirohiko; Okuno, Kazutoshi; Yano, Masahiro (2009-08-21). "Loss of Function of a Proline-Containing Protein Confers Durable Disease Resistance in Rice". Science. 325 (5943): 998–1001. doi:10.1126/science.1175550. ISSN 0036-8075.
  22. ^ Xiao, Ning; Wu, Yunyu; Pan, Cunhong; Yu, Ling; Chen, Yu; Liu, Guangqing; Li, Yuhong; Zhang, Xiaoxiang; Wang, Zhiping; Dai, Zhengyuan; Liang, Chengzhi (2017-01-03). "Improving of Rice Blast Resistances in Japonica by Pyramiding Major R Genes". Frontiers in Plant Science. 7. doi:10.3389/fpls.2016.01918. ISSN 1664-462X.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  23. ^ Cheong, Yong-Hwa; Kim, Min-Chul (2010-06-30). "Functions of MAPK Cascade Pathways in Plant Defense Signaling". The Plant Pathology Journal. 26 (2): 101–109. doi:10.5423/ppj.2010.26.2.101. ISSN 1598-2254.
  24. ^ Ramamoorthy, Rengasamy; Jiang, Shu-Ye; Kumar, Nadimuthu; Venkatesh, Prasanna Nori; Ramachandran, Srinivasan (2008). "A Comprehensive Transcriptional Profiling of the WRKY Gene Family in Rice Under Various Abiotic and Phytohormone Treatments". Plant and Cell Physiology. 49 (6): 865–879. doi:10.1093/pcp/pcn061. ISSN 1471-9053.
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