Open Access is an initiative that aims to make scientific research freely available to all. To date our community has made over 100 million downloads. It’s based on principles of collaboration, unobstructed discovery, and, most importantly, scientific progression. As PhD students, we found it difficult to access the research we needed, so we decided to create a new Open Access publisher that levels the playing field for scientists across the world. How? By making research easy to access, and puts the academic needs of the researchers before the business interests of publishers.
We are a community of more than 103,000 authors and editors from 3,291 institutions spanning 160 countries, including Nobel Prize winners and some of the world’s most-cited researchers. Publishing on IntechOpen allows authors to earn citations and find new collaborators, meaning more people see your work not only from your own field of study, but from other related fields too.
To purchase hard copies of this book, please contact the representative in India:
CBS Publishers & Distributors Pvt. Ltd.
www.cbspd.com
|
customercare@cbspd.com
Jilin Academy of Agricultural Sciences, Changchun, China
Jianbing Ma
University of Arkansas Rice Research and Extension Center, Stuttgart, Arkansas, USA
Tracy Bianco
USDA ARS Dale Bumpers National Rice Research Center, Stuttgart, Arkansas, USA
Yulin Jia*
USDA ARS Dale Bumpers National Rice Research Center, Stuttgart, Arkansas, USA
*Address all correspondence to: yulin.jia@ars.usda.gov
1. Introduction
1.1. The historical and contemporary aspects of rice blast disease
Rice (Oryza sativa L.) is one of the most important staple foods that feed more than half of the world’s population, with Asia and Africa as the largest consuming regions [1]. Blast disease caused by Magnaporthe oryzae (Hebert) Barr is one of the most damaging diseases of rice. This disease was first known as rice fever disease in China as early as 1637 [2]. Blast disease was first reported in the United States in 1876, and has been identified in 85 rice-producing countries or regions worldwide (Figure 1).
Blast severely affects lowland rice in temperate and subtropical areas of Asia, and is highly destructive to upland rice in tropical areas of Asia, Latin America, and Africa [3]. Although blast is considered the most destructive rice disease due to the favorable environmental conditions for disease occurrence and worldwide distribution, little information about annual yield losses are available. Table 1 summarizes reported blast outbreaks with annual yield losses from five countries. In China, 40-50% yield losses were observed under severe rice blast infection; in some cases, 100% yield losses were found in severely infected fields [4]. Yield losses of 5-10%, 8%, and 14% were reported in India from 1960 to 1961, Korea from the mid-1970s, and China from 1980 to 1981, respectively [3]. The highest yield losses were recorded in the Philippines; ranging from 50% to 85% in 1963 [3]. It was estimated that 1.6 billion dollars were lost from 1975-1990 due to blast disease worldwide [5]. The estimated annual loss of rice was enough to feed 60 million people for one year [6] (Table 1).
Figure 1.
Worldwide distribution of rice blast disease. Red dots show the countries or regions where blast disease has been reported.
The most common symptoms in commercial rice fields induced by M. oryzae can be found on all the above ground parts of the rice plant at all growth stages. Seeds display brown spots after infection, which may have resulted from the infection of the florets as they mature into seeds. Infected roots have also been observed; however, lesions on the sheaths were relatively rare. Infections on young seedlings are initiated when the conidia are deposited on the surface of the leaves. Water is essential for spores to germinate and attach to the leaf surface [7, 8]. Under optimal conditions, spore germination occurs rapidly and the polarized germ tubes are formed within hours after landing on the leaf [9]. The secondary cycles are initiated by the spores produced by the lesions on the young seedlings, which can be repeated many times through the growing season. Thousands of spores can be produced from a single lesion in 15 days after infection. Typically blast lesions are diamond shaped (Figure 2A). Initial lesions appear dark green or grey with brown borders; while, older lesions are light tan with necrotic borders. Under favorable conditions, lesions can merge together and rapidly enlarge to several centimeters in length, eventually killing the leaf, and ultimately resulting in plant death. On resistant cultivars, lesions induced by M. oryzae usually remain small in size (1-2mm) and appear brown to dark brown in color. Disease severity of rice blast and the amount of spores produced on single lesion depends on temperature, field conditions, relative humidity, fertilization levels, and genotype of rice cultivars. In general, moderate temperatures (~24°C), high relative humidity (90-92%), and high moisture with at least a 12-hour period are advantageous for rice blast. The disease severity of the vegetative phase during the growing season highly influences the amount of disease during the reproductive phase. Spores produced at the end of the growing season may result in collar blast and neck blast; neck blast often causes direct crop loss (Figure 2B).
Figure 2.
Symptoms of leaf (A) and neck blast diseases (B) in commercial rice fields.
Existence of physiological races of M. oryzae complicates the identification of resistance (R) genes. Physiological races of M. oryzae were first reported by Sasaki in Japan as early as 1922 [10]. From 1950s to 60s differential rice lines resistant to races of M. oryzae were identified in Japan, the United States, India, the Philippines, and South Korea. In 1961, 18 physiological races of M. oryzae were identified with 12 differential rice varieties in Japan. During that time, an international differential system using 8 rice varieties was established [11]. In China, the identification of M. oryzae races was initiated in late 1970s. Seven rice varieties, Tebo, Zhenlong13, Sifeng43, Dongnong363, Kanto51, Hejiang18, and Lijiangxintuanheigu (LTH), and 43 isolates of M. oryzae were used. In 1976, Yamada and his colleagues identified 23 races ofM. oryzae from 2245 isolates with 9 differential rice varieties. Duan et al [12] used Yuyun 1 (with Pia), Gaoliangdao (with Pii), Kanto51 (with Pik), Chugeng1 (with Pikm), Dianyu1 × Fook Kam (with Piz), Dali782 (with Pita), Dan83-3 (with Pita2), and Chengbao1 (withPizt) as differential varieties to characterize races ofM. oryzae in China. These blast R genes are described in more details in the part II of this chapter. Near-isogenic lines (NILs) were chosen to better identify races ofM. oryzae in a gene-for-gene specific manner. The NILs with indica high-susceptible variety CO39 background was developed at the International Rice Research Institute (IRRI), the Philippines [13]. In the United States, Marchetti [14] reported that the races IB-54, ID-13, IG-1, and IH-1 of M. oryzae were the most common. Most recently, monogenic lines with 24 major blast R genes in BC1 of LTH were developed by scientists at IRRI and Japan [15].
Extensive analysis of rice germplasm with physiological races in the past century reveals that complete genetic resistance (vertical resistance) is conferred by major blast R genes named as Piricularia genes or Pi-genes. These genes are often specific in preventing infections by strains of M. oryzae that contain the corresponding avirulence genes; whereas, incomplete resistance (slow-blasting components or horizontal resistance, field resistance, or dilatory resistance) is often conditioned by more than one gene on different chromosomal regions. These genes are referred to as quantitative resistant loci (QTLs). Resistant germpalsms carrying both major and minor R genes and are extremely important genetic resources that rice breeders can use to improve blast resistance in elite rice varieties.
Blast R genes are predicted to play important roles in the frontier of rice defense responses. During interactions between rice and blast pathogens, products of the R gene can specifically recognize the corresponding elicitors of M. oryzae. Since the Pia gene, indentified in 1967 by Kiyosawa as the first blast R gene from the japonica variety Aichi Asahi [16], 99 blast R genes have been identified; in which 45% were found in japonica cultivars, 51% in indica cultivars, and the rest 4% in wild rice species (Table 2 to 5). Most deployed R genes have often been identified in Asian cultivated rice, specially rice cultivars from Japan and China, with the exception of Pi9, Pi54rh, Pi40(t), and Pirf2-1(t), which were domesticated from O. minuta, O. rhizomatis, O. australiensis, and O. rufipogon, respectively. All R genes have been mapped on all rice chromosomes except for chromosome 3 (Tables 2 to 4; Fig 3). Host genotypes, chromosomal loci, and molecular markers that are tightly linked to blast R genes are summarized in Figure 2 and Table 2 (60 major R gene) and Table 3 (17 minor R gene). Among them, three major R gene clusters have been well characeterized: the Piz locus on Chromosome 6, the Pik locus on Chromosome 11, and the Pita locus on Chromosome 12 (Figure 3). More detailed imformation of mapped blast R genes can be found at http://www.ricedata.cn/gene/, http://www.shigen.nig.ac.jp/rice/oryzabaseV4/, and http://www.gramene.com.
Chromosome
Major R genes mapped*
Minor R genes mapped*
R gene cloned*
Total*
1
2
2
3
7
2
7
3
1
11
3
0
0
0
0
4
1
2
1
4
5
2
1
0
3
6
12
1
6
19
7
1
0
0
1
8
4
2
1
7
9
3
0
1
3
10
1
1
0
2
11
12
3
8
23
12
15
2
1
18
Total
60
17
22
99
Table 2.
Summary of blast R (major and minor, mapped and cloned) genes on rice chromosomes.
* refers to number of the genes on the chromosome.
Summary of major blast R genes including their resistance specificity, chromosomal location, map position, and tightly linked DNA markers.
* This R gene shares the same name with another R gene.
# The map positions were integrated into IRGSP map according to marker information. Detail information can be found on http://rgp.dna.affrc.go.jp/E/IRGSP/index.html.
‡ Information is known, but has not been published.
Summary of minor blast R genes, donors, map position, tightly linked DNA markers, and associated blast races.
* This R gene shares the same name with another R gene.
# The map positions were integrated into IRGSP map according to marker information. Detail information can be found on http://rgp.dna.affrc.go.jp/E/IRGSP/index.html.
Figure 3.
Location of cloned and mapped R genes on rice chromosomes. The locations of R genes have been integrated into IRGSP map according to marker information, then the map was built using Mapmaker software. Centimorgan was used to measure the map positions showing in the right column of the choromosome. The underlined words indicate either SSR or RFLP markers (see additional resources: http://www.shigen.nig.ac.jp/rice/oryzabaseV4/insd/detail/3554).
Summary of cloned R genes, map position, closely linked DNA markers, and their expression.
* This R gene shares the same name with another R gene. # The map positions were integrated into IRGSP map according to marker information. Detail information can be found on http://rgp.dna.affrc.go.jp/E/IR.
Among the mapped R genes (Table 3 and 4), 22 genes including 20 major and 2 minor R genes (Pb1 and pi21) have been molecularly characterized (Table 5). Noticeably, Pid2, Pid3, Pi36, Pb1, and Pita are single copy genes; while others are members of small gene families. A total of eight R genes have been identified on chromosome 11, with six at the Pik locus; six R genes on chromosome 6, four of which are at the Piz locus. Most cloned blast R genes are adequate in providing complete resistance to strains of M. oryzae that contain the corresponding avirulence genes. Interestingly, two different members of each of Pi5, Pik, Pikp, Pikm, and Pia are required for complete resistance to some avirulent races.
Figure 4.
Structure of all cloned R genes. The light green bar represents the length of the R genes. The highlighted bars represent the different domains of the R genes.
Similar to other plant R genes, all cloned blast R genes to date encode predicted proteins with centrally located nucleotide binding sites (NBS) and leucine rich repeat (LRR) at the carboxyl terminus (Figure 4), with the exception of Pid2 and pi21 encoding a B-lectin kinase protein and a proline containing protein, respectively. Plant NBS-LRR proteins can be divided into two subgroups based on whether they contain a Toll-interleukin receptor (TIR)-like domain (TIR-NBS-LRR) or a putative coiled-coil (CC) structure (CC-NBS-LRR) in their amino-terminal region. The rice genome has 500 NBS-LRR gene families, and most of them belong to the CC-NBS-LRR family. The NBS domain contains kinase 1a (p-loop), kinase 2 and 3a (RNBS-B) motif, which presumably bind to ATP and trigger downstream signal transduction; whereas, the LRR is predicted to recognize pathogen effectors, either directly or indirectly. Other noticeable protein domains of plant R proteins were also summarized in Figure 4.
The observed structural similarities of blast R proteins might imply that their predicted conserved regions are associated with functional roles in triggering resistance to M. oryzae. Cloned blast R genes can be separated into two clades, I and II (Figure 5). Clade I consists of all NBS-LRR genes and clade II contains both NBS-LRR and non-NBS-LRR gene, such as Pid2 and pi21. Among them, Pi1-5, Pik-1, Pikp-1, and Pikm1-TS on chromosome 11 share substantial homology to the Pi9 locus on Chromosome 6; whereas, Pi1-6, Pik-2, Pikp-2, and Pikm2-T are more similar to Pid2 and pi21, which are not NBS-LRR R genes. Homologous sequences of blast R genes can be found in the diverse germplasm of cultivated species including domesticated landrace varieties and wild relatives of rice. These observations suggest that genetics of rice immunity is ancient and may have been evolved during speciation and domestication.
Figure 5.
Phylogenetic tree of all cloned blast R genes. The tree was constructed using protein sequences by software Mega 5.0 NJ method.
4. R gene-mediated signaling transduction pathways
It is now commonly accepted that products of R genes in plants can specifically recognize avirulence genes from the pathogen directly or indirectly to initiate innate immunity system responses. Direct recognition of the putative product of the avirulence gene, AVR-Pita1 by the Pita protein was first reported in 2000 [93]. Over a decade later, in 2012, another blast R protein, Pik, with similar structure to Pita, was found to directly recognize the corresponding avirulence gene AvrPik [94]. Direct interactions between other blast R and avirulence genes have not been reported; suggesting that indirect interactions may be responsible in triggering effective signal transduction pathways. Other plant genes involved in signal transduction have been investigated by the use of R proteins as bait in the yeast two-hybrid system (Y2H). While Y2H is a highly effective tool, it is limited in indentifying immediate plant components of R proteins. Molecular basis of blast R gene-mediated signaling has been a subject of intensive investigation worldwide. Abundant genes that may be involved in R gene-mediated signaling have been identified with DNA microarray [95, 96], and most of them were pathogenicity related genes. Genetic analysis using mutagenesis has been another commonly used alternative to identify downstream components. However, most mutants identified, thus far, are lesion mimic mutants [97]. A major effort to identify Pita mediated signaling was accomplished by treating 20,000 Katy seeds with Pita/Pita2/Piks using fast neutrons, ethyl methyl sulfate (EMS), and gamma irradiation [98]. A total of 142 rice seedlings, with altered disease reactions, were identified from independent M2. The susceptibility of M2 individuals was verified in subsequent generations, and 20 of them were confirmed to be derived from Katy using 20 diagnostic single sequence repeat (SSR) markers. Consequently, the Ptr(t) gene in rice was identified to be essential for Pita mediated signal transudation [99]. Molecular cloning of Ptr(t) will shed light on the interaction mechanism of Pita and Ptr(t), and subsequent plant genes involved in defense responses.
5. The management of blast disease-marker assisted selection
Blast disease has been effectively managed by a combination of fungicides and R genes integrated into diverse cultural practices. These include seed treatment with fungicide; preventive application of fungicide before heading; crop rotation; balanced application of fertilizers with nitrogen, potassium, and phosphate; and maintaining a sufficient water level during tillering and flowering stages. However, the most effective way to manage rice blast is by the utilization of resistant cultivars due to its environmental and economic sustainability. Incorporating major blast R genes have been traditionally accomplished by classical breeding methods and can be accelerated by the use of marker assisted selection (MAS) [100]. MAS has become a practical tool in cultivar improvement by selecting important traits at the early growth stages based on DNA markers, thus breeders can screen for resistance without having to maintain pathogen culture. MAS is efficient and consistent in the field and greenhouse [101]. MAS is also reliable in dealing with traits whose phenotype is affected by the environment. To date, 99 blast R genes have been mapped with closely linked DNA markers; and some of them can be used for MAS. DNA markers were also developed from portions of cloned R genes, such as Pi-ta and Pi-b, for their introduction into elite rice cultivars using MAS. Markers for Pita, one of the most important R genes for blast in the United States, were developed [102]; while, linked markers for 4 blast R genes (Pik, Pib, Pita2, and Pii) are effective against eight to ten races of M. oryzae were identified [103]. Using MAS, R genes like Pi1, Pi5, Piz-5, and Pita have been established in different rice genotypes [82, 100, 104, 105]
Blast disease is a moving target where the fungus can rapidly adapt to the host. The major difficulty in controlling rice blast is the durability of genetic resistance. Rice cultivars containing only a single R gene to a specific pathogen race often become susceptible over time due to the emergence of new virulent races. In theory, R genes can be found in rice germplasm in different rice production areas. Stacking R genes with overlapped resistance spectra can lead to long lasting resistance. Knowledge of genetic identity of contemporary M. oryzae is crucial for precise deployment of rice cultivars with different R genes [104]. Effective blast management also requires unprecedented international cooperation. IRRI and research institutions worldwide have been coordinating their resources for both genotyping using next generation of DNA sequencing and phenotyping at different geographic locations. The knowledge gained by this massive collaborative effort ought to lead to more effective methods to reduce crop loss due to blast disease worldwide.
We thank the Arkansas Rice Research and Promotion Board, and the US National Science Foundation (Plant Research Program no. 0701745), Natural Science Foundation of China (Program no. 31000847), Zhejiang Natural Science Foundation (Program no. Y3100577), and Qianjiang Talents Project supported by Science Technology Department of Zhejiang Province (Program no. 2011R10038) for their partial financial supports. USDA is an equal opportunity provider and employer.
References
1.United States Department of Agriculture-Economic Research Service. USDA-ERS: Topics, Crops: rice. http://www.ers.usda.gov/topics/crops/rice/background (Accessed 20 September 2012)
4.Zhang L, Zhang Q, Cheng Z, Yang H, Zhou Y, Lu C. Resistances of four sets of rice varieties to 19 strains of Magnaporthe grisea in Jiangsu area. Jiangsu Journal of Agricultural Science 2010; 26(5) 948-953.
6.Pennisi E. Armed and dangerous. Science 2010; 327 (5867) 804-805.
7.Hamer JE, Howard RJ, Chumley FG, Valent B. A mechanism for surface attachment in spores of a plant pathogenic fungus. Science 1988; 239(4837) 288-290.
8.Bourett TM, Howard RJ. In vitro development of penetration structures in the rice blast fungus Magnaporthe grisea. Canadian Journal of Botany 1990; 68(2) 329-432.
9.Talbot NJ. On the Trail of a Cereal Killer: Exploring the biology of Magnaporthe grisea. Annual Review of Microbiology 2003; 57(1) 177-202.
10.Sasaki R. Extensive of strains in rice blast fungus. Journal of plant protection 1992; 9 634-644
11.Ling KC, Ou SH. Standardization of the international race numbers of Pyricularia oryzae. Phytopathology 1969; 59 339-342.
12.Duan Y, Zhu Y, Chen H, Na X. The blast resistance mechanisms and genetic regularity. Journal of Yunnan Agricultural University 1987; 2(2) 11-16.
13.Mackill DJ, Bonman JM. Inheritance of blast resistance in near isogenic lines of rice. Phytopathology 1992; 82 (7) 746-749.
14.Marchetti MA. Race-specific and rate-reducing resistance to rice blast in US rice cultivars. In: Zeigler RS, Leong SA, Teng PS (eds.) Rice blast disease. Wallingford: Cab International; 1994. pp 231-244.
15.Tsunematsu H, Yanoria MJT, Ebron LA, Hayashi N, Ando I, Kato H, Imbe T, Khush GS. Development of Monogenic Lines of Rice for Rice Blast Resistance. Breeding Science 2000; 50(3) 229-234.
16.Kiyosawa, S.. Genetic studies on host–pathogen relationship in the rice blast disease. In: Ogura T. (ed.) 1967: rice disease and their control by growing resistant varieties and other measures: proceedings of the Symposium of Agriculture, Forestry and Fisheries Research Council, 1967, Tokyo, Japan.
17.Zhu M, Wang L, Pan Q. Identification and characterization of a new blast resistance gene located on rice chromosome 1 through linkage and differential analyses. Phytopathology 2004; 94(5) 515-519.
18.Barman SR, Gowda M, Venu RC, Chattoo BB. Identification of a major blast resistance gene in the rice cultivar 'Tetep'. Plant Breeding 2004; 123(3) 300-302.
19.Pan Q, Wang L, Ikehashi H, Yamagata H, Tanisaka T. Identification of two new genes conferring resistance to rice blast in the Chinese native cultivar ‘Maowangu’. Plant breeding 1998; 117(1) 27-31.
20.Pan Q, Wang L, Tanisika T. A new blast resistance gene identified in the Indian native rice cultivar Aus373 through allelism and linkage tests. Plant Pathology Journal 1999; 48(2) 288-293.
21.Shi B, Zhang J, Zheng Y, Liu Y, Vera Cruz C, Zheng T, Zhao M. Identification of a new resistance gene Pi-Da(t) from Dacca6 against rice blast fungus (Magnaporthe oryzae) in Jin23B background. Molecular Breeding 2012; 30(2)1089-1096.
22.Chen X, Li S, Xu J, Zhai W, Ling Z, Ma B, Wang Y, Wang W, Cao G, Ma Y, Shang J, Zhao X, Zhou K, Zhu L. Identification of two blast resistance genes in a rice variety, Digu. Journal of Phytopathology 2004; 152(2) 77-85.
23.Tabien RE, Li Z, Paterson AH, Marchetti MA, Stansel JW, Pinson SRM. Mapping of four major rice blast resistance genes from 'Lemont' and 'Teqing' and evaluation of their combinatorial effect for field resistance. Theoretical and Applied Genetics 2000; 101(8)1215-1225.
24.Zhou J, Wang J, Xu J, Lei C Ling Z. Identification and mapping of a rice blast resistance gene Pi-g(t) in the cultivar Guangchangzhan. Plant pathology 2004; 53(2) 191-196.
25.Lei C, Huang D, Li W, Wang J, Liu Z, Wang X, Shi K, Cheng Z, Zhang X, Ling Z, Wan J. Molecular mapping of a blast resistance gene in an indica rice cultivar Yanxian No.1. Rice Genetics Newsletter 2005; 22 76-77.
26.Terashima T, Fukuoka S, Saka N, Kudo S. Mapping of a blast field resistance gene Pi39(t) of elite rice strain Chubu 111. Plant Breeding 2008; 127(5) 485-489.
27.Naqvi NI, Bonman JM, Makill DJ, Nelson RJ, Chattoo BB. Identification of RAPD markers linked to major blast resistance gene in rice. Molecular Breeding 1995;1(4) 341-348.
28.Ahn SN, Kim YK, Hong HC, Han SS, Choi HC, McCouch SR, Moon HP. Mapping of genes conferring resistance to Korean isolates of rice blast fungus using DNA markers. Korean Journal of Breeding 1997; 29(4) 416-423.
29.Wang Y, Wang D, Deng X, Liu J, Sun P, Liu Y, Huang H, Jiang N, Kang H, Ning Y, Wang Z, Xiao Y, Liu X, Liu E, Dai L, Wang G. Molecular mapping of the blast resistance genes Pi2-1 and Pi51(t) in the durably resistant rice 'Tianjingyeshengdao'. Phytopathology 2012; 102(8) 779-786.
30.Jiang N, Li Z, Wu J, Wang Y, Wu L, Wang S, Wang D, Wen T, Liang Y, Sun P, Liu J, Dai L, Wang Z, Wang C, Luo M, Liu X, Wang G. Molecular mapping of the Pi2/9 allelic gene Pi2-2 conferring broad-spectrum resistance to Magnaportheoryzae in the rice cultivar Jefferson. Rice 2012; 5(29) 1-7.
31.Pan Q, Wang L, Ikehashi H,Taniska T. Identification of a new blast resistance gene in the indica rice cultivar Kasalath using Japanese differential cultivars and isozyme markers. Phytopathology 1996; 86(10) 1071-1076.
32.Ebitani T, Hayashi N, Omoteno M, Ozaki H, Yano M, Morikawa M, Fukuta Y. Characterization of Pi13, a blast resistance gene that maps to chromosome 6 in indica rice (Oryzasativa L. variety, Kasalath). Breeding Science 2011; 61(3) 251-259.
33.Wu J, Fan Y, Li D, Zheng K, Leung H, Zhuang J. Genetic control of rice blast resistance in the durably resistant cultivar Gumei 2 against multiple isolates. Theoretical and Applied Genetics 2005; 111(1) 50-56.
34.Jeung JU, Kim BR, Cho YC, Han SS, Moon HP, Lee YT, Jena KK. A novel gene, Pi40(t), linked to the DNA markers derived from NBS-LRR motifs confers broad spectrum of blast resistance in rice. Theoretical and Applied Genetics 2007; 115 (8) 1163-1177.
35.Zhu X, Chen S, Yang J, Zhou S, Zeng L, Han J, Su J, Wang L, Pan Q. The identification of Pi50(t), a new member of the rice blast resistance Pi2/Pi9 multigene family. Theoretical and Applied Genetics 2012; 124(7) 1295-1304.
36.Deng Y, Zhu X, Shen Y, He Z. Genetic characterization and fine mapping of the blast resistance locus Pigm(t) tightly linked to Pi2 and Pi9 in a broad-spectrum resistant Chinese variety. Theoretical and Applied Genetics 2006; 113(4) 705-713.
37.Hayashi K, Hashimoto N, Daigen M, Ashikawa I. Development of PCR-based SNP markers for rice blast resistance genes at the Piz locus. Theoretical and Applied Genetics 2004; 108(7) 1212-1220.
38.Pan Q, Tanisaka T, Ikehashi H. Studies on the genetics and breeding of blast resistance in rice VI. Gene analysis for the blast resistance of two Yunnan native cultivars GA20 and GA25. Breeding Science 1996; 46(Suppl 2) 70.
39.Lee S, Wamishe Y, Jia Y, Liu G, Jia M. Identification of two major resistance genes against race IE-1k of Magnaporthe oryzae in the indica rice cultivar Zhe733. Molecular Breeding 2009; 24(2) 127-134.
40.Berruyer R, Adreit H, Milazzo J, Gaillard S, Berger A, Dioh W, Lebrun MH, Tharreau D. Identification and fine mapping of Pi33, the rice resistance gene corresponding to the Magnaporthe grisea avirulence gene ACE1. Theoretical and Applied Genetics 2003; 107(6) 1139-1147.
41.He X, Liu X, Wang L, Wang L, Lin F, Cheng Y, Chen Z, Pan Q. Identification of the novel recessive gene pi55(t) conferring resistance to Magnaportheoryzae. Science China Life Sciences 2012; 55(2) 141-150.
42.Liu B, Zhang S, Zhu X, Yang Q, Wu S, Mei M, Mauleon R, Leach J, Mew T, Leung H. Candidate defense genes as predictors of quantitative blast resistance in rice. Molecular Plant-Microbe Interactions 2004; 17(10) 1146-1152.
43.Jeon J S, Chen D, Yi G, Wang G, Ronald PC. Genetic and physical mapping of Pi5(t), a locus associated with broad-spectrum resistance to rice blast. Molecular Genetics and Genomics 2003; 269(2) 280-289.
44.Lin F, Liu Y, Wang L, Liu X Pan Q. A high-resolution map of the rice blast resistance gene Pi15 constructed by sequence-ready markers. Plant Breeding 2007; 126(3) 287-290.
45.Ahn SH, Kim YK, Hong HC, Han SS, Kwon SJ, Choi HC, Moon HP, McCouch SR. Molecular mapping of a new gene for resistance to rice blast (Pyricularia grisea Sacc.). Euphytica 2000; 116(1) 17-22.
46.Gowda M, Roy-Barman S, Chattoo BB. Molecular mapping of a novel blast resistance gene Pi38 in rice using SSLP and AFLP markers. Plant Breeding 2006; 125(6) 596-599.
47.Chen D, dela Viña M, Inukai T, Mackill DJ, Ronald PC, Nelson RJ. Molecular mapping of the blast resistance gene, Pi44(t), in a line derived from a durably resistant rice cultivar. Theoretical and Applied Genetics 1999; 98 1046-1053.
48.Chauhan RS, Farman ML, Zhang HB, Leong SA. Genetic and physical mapping of a rice blast resistance locus, Pi-CO39(t), that corresponds to the avirulence gene AVR1-CO39 of Magnaporthegrisea. Molecular Genetics and Genomics 2002; 267(5) 603-612.
49.Campbell MA, Chen D, Ronald PC. Development of co-dominant amplified polymorphic sequence markers in rice that flank the Magnaporthe grisea resistance gene Pi7(t) in recombinant inbred line 29. Phytopathology 2004; 94(3) 302-307
50.Huang H, Huang L, Feng G, Wang S, Wang Y, Liu J, Jiang N, Yan W, Xu L, Sun P, Li Z, Pan S, Liu X, Xiao Y, Liu E, Dai L, Wang G. Molecular mapping of the new blast resistance genes Pi47 and Pi48 in the durably resistant local rice cultivar Xiangzi 3150. Phytopathology 2011; 101(5) 620-626.
51.Fjellstrom R, Conaway-Bormans CA, McClung AC, Marchetti MA, Shank A, Park WD. Development of DNA markers suitable for marker assisted selection of three Pi-genes conferring resistance to multiple Pyricularia grisea pathotypes. Crop Science 2004; 44(5) 1790-1798.
52.Zhang J, Wang G, Xie H, Ling Z. Genetic analysis and mapping of blast resistance genes in japonica rice Yunyin from Yunnan provice. Journal of Agricultural Biotechnology 2003; 11(3) 241-244.
53.Zhang J, Tan Y, Hong R, Fan J, Luo Q, Zeng Q. Genetic analysis and gene mapping of rice blast resistance in japonica variety Ziyu 44. Chinese journal of rice science 2009; 23(1) 31-35.
54.Koide Y, Telebanco-Yanoria MJ, dela Peña FD, Fukuta Y, Kobayashi N. Characterization of rice blast isolates by the differential system and their application for mapping a resistance gene, Pi19(t). Journal of Phytopathology 2011; 159(2) 85–93.
55.Causse MA, Fulton TM, Cho YG, Ahn SN, Chunwongse J, Wu K, Xiao J, Yu Z, Ronald PC, Harrington SE, Second G, McCouch SR, Tanksley SD. Saturated molecular map of the rice genome based on an interspecific backcross population. Genetics 1994; 138(4)1251-1274.
56.Wu KS, Martinez C, Lentini Z, Tohme J, Chumley FG, Scolnik PA, Valent B. Cloning a blast resistance gene by chromosome walking. In: Khush GS. (ed.) IRRI1996: map-based gene cloning: proceedings of the Third International Rice Genetic Symposium, IRRI, 1996, Manila, Philippines.
57.Zhuang J, Ma W, Wu J, Chai R, Lu J, Fan Y, Jin M, Leung H, Zheng K. Mapping of leaf and neck blast resistance genes with resistance gene analog, RAPD and RFLP in rice. Euphytica 2002; 128(3) 363-370
58.Inukai T, Zeigler RS, Sarkarung S, Bronson M, Dung LV, Kinoshita T, Nelson RJ. Development of pre-isogenic lines for rice blast-resistance by marker-aided selection from a recombinant inbred population. Theoretical and Applied Genetics 1996; 93(4) 560-567.
59.Liu X, Yang Q, Lin F, Hua L, Wang C, Wang L, Pan Q. Identification and fine mapping of Pi39(t), a major gene conferring the broad-spectrum resistance to Magnaporthe oryzae. Molecular Genetics and Genomics 2007; 278(4) 403-410.
60.Yang Q, Lin F, Wang L, Pan Q. Identification and mapping of Pi41, a major gene conferring resistance to rice blast in the Oryza sativa subsp. indica reference cultivar, 93-11. Theoretical and Applied Genetics 2009; 118(6) 1027-1034.
61.Naqvi NI, Chattoo BB. Development of a sequence characterized amplified region (SCAR) based indirect selection method for a dominant blast-resistance gene in rice. Genome 1996; 39(1) 26-30.
62.Zheng K, Qiang H, Zhuang J, Lu J, Lin H. Mapping of rice resistance genes to blast using DNA marker. Acta Phytopathologica Sinica 1995; 25(4) 307-313.
63.Sallaud C, Lorieux M, Roumen E, Tharreau D, Berruyer R, Svestasrani P, Garsmeur O, Ghesquiere A, Notteghem JL. Identification of five new blast resistance genes in the highly blast-resistant rice variety IR64 using a QTL mapping strategy. Theoretical and Applied Genetics 2003; 106(5) 794-803.
64.Nguyen TT, Koizumi S, La TN, Zenbayashi KS, Ashizawa T, Yasuda N, Imazaki I, Miyasaka A. Pi35(t), a new gene conferring partial resistance to leaf blast in the rice cultivar Hokkai 188. Theoretical and Applied Genetics 2006; 113(4) 697-704.
65.Utami DW, Moeljopawiro S, Aswidinnoor H, Setiawan A, Hanarida I. Blast resistance genes in wild rice Oryza rufipogon and rice cultivar IR64. Indonesian Journal of Agriculture 2008; 1(2) 71-76
66.Goto I. Genetic studies on resistance of rice plant to blast fungus (VII). Blast resistance genes of Kuroka. Annals of Phytopathological Society of Japan 1988; 54 460-465.
67.Xu X, Chen H, Fujimura T, Kawasaki S. Fine mapping of a strong QTL of field resistance against rice blast, Pikahei-1(t), from upland rice Kahei, utilizing a novel resistance evaluation system in the greenhouse. Theoretical and Applied Genetics 2008; 117(6) 997-1008.
68.Wang G, Mackill D, Bonman J, McCouch SR, Champoux MC, Nelson RJ. RFLP mapping of genes conferring complete and partial resistance to blast in a durably resistance rice cultivar. Genetics 1994; 136(4) 1421-1434.
69.Zenbayashi-Sawata K, Fukuoka S, Katagiri S, Fujisawa M, Matsumoto T, Ashizawa T, Koizumi S. Genetic and physical mapping of the partial resistance gene, pi34, to blast in rice. Phytopathology 2007; 97(5) 598-602.
70.Toriyama K. Breeding for resistance to major rice disease in Japan. In: IRRI (ed.) Rice Breeding. Manila: IRRI; 1972. p253-281.
71.Hayashi K, Yoshida H. Refunctionalization of the ancient rice blast disease resistance gene Pit by the recruitment of a retrotransposon as a promoter. The Plant Journal 2009; 57(3) 413-425.
72.Lin F, Chen S, Que Z, Wang L, Liu X, Pan Q. The blast resistance gene Pi37 encodes a nucleotide binding site leucine-rich repeat protein and is a member of a resistance gene cluster on rice chromosome 1. Genetics 2007; 177(3) 1871-1880.
73.Takahashi A, Hayashi N, Miyao A, Hirochika H. Unique features of the rice blast resistance Pish locus revealed by large scale retrotransposon-tagging. BMC Plant Biology 2010; 10175.
74.Wang Z, Yano M, Yamanouchi U, Iwamoto M, Monna L, Hayasaka H, Katayose Y, Sasaki T. The Pib gene for rice blast resistance belongs to the nucleotide binding and leucine-rich repeat class of plant disease resistance genes. The Plant Journal 1999; 19(1) 55-64.
75.Fukuoka S, Saka N, Koga H, Ono K, Shimizu T, Ebana K, Hayashi N, Takahashi A, Hirochika H, Okuno K,Yano M. Loss of function of a proline-containing protein confers durable disease resistance in rice. Science 2009; 325(5943) 998-1001.
76.Chen X, Shang J, Chen D, Lei C, Zou Y, Zhai W, Liu G, Xu J, Ling Z, Cao G, Ma B, Wang Y, Zhao X, Li S, Zhu L. A B-lectin receptor kinase gene conferring rice blast resistance. The Plant Journal 2006; 46(5) 794-804.
77.Qu S, Liu G, Zhou B, Bellizzi M, Zeng L, Dai L, Han B, Wang G. The broad-spectrum blast resistance gene Pi9 encodes a nucleotide-binding site-leucine-rich repeat protein and is a member of a multigene family in rice. Genetics 2006; 172(3) 1901-1914.
78.Zhou B, Qu S, Liu G, Dolan M, Sakai H, Lu G, Bellizzi M, Wang G. The eight amino-acid differences within three leucine-rich repeats between Pi2 and Piz-t resistance proteins determine the resistance specificity to Magnaporthegrisea. Molecular Plant-Microbe Interactions 2006; 19(11) 1216-1228.
79.Shang J, Tao Y, Chen X, Zou Y, Lei C, Wang J, Li X, Zhao X, Zhang M, Lu Z, Xu J, Cheng Z, Wan J, Zhu L. Identification of a new rice blast resistance gene, Pid3, by genomewide comparison of paired nucleotide-binding site--leucine-rich repeat genes and their pseudogene alleles between the two sequenced rice genomes. Genetics 2009; 182(4) 1303-1311.
80.Chen J, Shi Y, Liu W, Chai R, Fu Y, Zhuang J, Wu J. A Pid3 allele from rice cultivar Gumei2 confers resistance to Magnaportheoryzae. Journal of Genetics and Genomics 2011; 38(5) 209-216.
81.Liu X, Lin F, Wang L, Pan Q. The in silico map-based cloning of Pi36, a rice coiled-coil nucleotide-binding site leucine-rich repeat gene that confers race-specific resistance to the blast fungus. Genetics 2007; 176(4) 2541-2549.
82.Lee SK, Song MY, Seo YS, Kim HK, Ko S, Cao PJ, Suh JP, Yi G, Roh JH, Lee S, An G, Hahn TR, Wang GL, Ronald P, Jeon JS. Rice Pi5-mediated resistance to Magnaportheoryzae requires the presence of two coiled-coil-nucleotide-binding-leucine-rich repeat genes. Genetics 2009; 181(4) 1627-1638.
83.Hua L, Wu J, Chen C, Wu W, He X, Lin F, Wang L, Ashikawa I, Matsumoto T, Wang L, Pan Q. The isolation of Pi1, an allele at the Pik locus which confers broad spectrum resistance to rice blast. Theoretical and Applied Genetics 2012; 125(5) 1047-1055.
84.Zhai C, Lin F, Dong Z, He X, Yuan B, Zeng X, Wang L, Pan Q. The isolation and characterization of Pik, a rice blast resistance gene which emerged after rice domestication. New Phytologist 2011;189(1) 321-334.
85.Ashikawa I, Hayashi N, Abe F, Wu J,Matsumoto T. Characterization of the rice blast resistance gene Pik cloned from Kanto51. Molecular Breeding 2012; 30(1) 485-494.
86.Ashikawa I, Hayashi N, Yamane H, Kanamori H, Wu J, Matsumoto T, Ono K, Yano M. Two adjacent nucleotide-binding site-leucine-rich repeat class genes are required to confer Pikm-specific rice blast resistance. Genetics 2008; 180(4) 2267-2276.
87.Yuan B, Zhai C, Wang W, Zeng X, Xu X, Hu H, Lin F, Wang L, Pan Q. The Pik-p resistance to Magnaporthe oryzae in rice is mediated by a pair of closely linked CC-NBS-LRR genes. Theoretical and Applied Genetics 2011; 122(5) 1017-1028.
88.Sharma TR, Madhav MS, Singh BK, Shanker P, Jana TK, Dalal V, Pandit A, Singh A, Gaikwad K, Upreti HC, Singh NK. High-resolution mapping, cloning and molecular characterization of the Pi-k(h) gene of rice, which confers resistance to Magnaporthegrisea. Molecular Genetics and Genomics 2005; 274(6) 569-578.
89.Das A, Soubam D, Singh PK, Thakur S, Singh NK,Sharma TR. A novel blast resistance gene, Pi54rh cloned from wild species of rice, Oryza rhizomatis confers broad spectrum resistance to Magnaporthe oryzae. Functional and Integrative Genomics 2012; 12(2) 215-228.
90.Okuyama Y, Kanzaki H, Abe A, Yoshida K, Tamiru M, Saitoh H, Fujibe T, Matsumura H, Shenton M, Galam DC, Undan J, Ito A, Sone T, Terauchi R. A multifaceted genomics approach allows the isolation of the rice Pia-blast resistance gene consisting of two adjacent NBS-LRR protein genes. The Plant Jounal 2011; 66(3) 467-479.
91.Hayashi N, Inoue H, Kato T, Funao T, Shirota M, Shimizu T, Kanamori H, Yamane H, Hayano-Saito Y, Matsumoto T, Yano M, Takatsuji H. Durable panicle blast-resistance gene Pb1 encodes an atypical CC-NBS-LRR protein and was generated by acquiring a promoter through local genome duplication. The Plant Journal 2010; 64(3) 498-510.
92.Bryan GT, Wu KS, Farrall L, Jia Y, Hershey HP, McAdams SA, Faulk KN, Donaldson GK, Tarchini R, Valent B. tA single amino acid difference distinguishes resistant and susceptible alleles of the rice blast resistance gene Pi-ta. The Plant Cell 2000; 12(11) 2033-2046.
93.Jia Y, McAdams SA, Bryan GT, Hershey HP, Valent B. Direct interaction of resistance gene and avirulence gene products confers rice blast resistance. EMBO Journal 2000; 19(15): 4004-4014.
94.Kanzaki H, Yoshida K, Saitoh H, Fujisaki K, Hirabuchi A, Alaux L, Fournier E, Tharreau D, Terauchi R. Arms race co-evolution of Magnaporthe oryzaeAVR-Pik and rice Pik genes driven by their physical interactions. The Plant Journal 2012; 72(6) 894-907.
95.Vergne E, Ballini E, Marques S, Sidi Mammar B, Droc G, Gaillard S, Bourot S, DeRose R, Tharreau D, Notteghem JL, Lebrun MH, Morel JB. Early and specific gene expression triggered by rice resistance gene Pi33 in response to infection by ACE1 avirulent blast fungus. New Phytologist 2007; 174(1) 159-171.
96.Gupta SK, Rai AK, Kanwar SS, Chand D, Singh NK, Sharma TR. The single functional blast resistance gene Pi54 activates a complex defence mechanism in rice. Journal of Experimental Botany 2012; 63(2) 757-772.
97.Jia Y. Registration of lesion mimic mutant of Katy rice. Crop Science 2005; 45(4) 1675.
98.Jia Y, Xie J, Rutger JN. Development and characterization of Katy deletion mutant populations. Plant Mutation Reports 2006; 1(1) 43-47.
99.Jia Y, Martin R. Identification of a new locus, Ptr(t), required for rice blast resistance gene Pi-ta-mediated resistance. Molecular Plant-Microbe Interactions 2008; 21(4) 396-403.
100.Hittalmani S, Parco A, Mew TV, Zeigler RS, Huang N. Fine mapping and DNA marker-assisted pyramiding of the three major genes for blast resistance in rice. Theoretical and Applied Genetics 2000; 100(7) 1121–1128.
101.Moose SP, Mumm RH. Molecular plant breeding as the foundation for 21st century crop improvement. Plant Physiology 2008; 147(3) 969-977.
102.Jia, Y, Wang, Z, Singh P. Development of dominant rice blast resistance Pi-ta gene markers. Crop Science 2002; 42(3) 2145-2149.
103.Jia, Y. Understanding the molecular mechanisms of rice blast resistance using rice mutants. In: Shu Q. (ed.) Induced Plant Mutations in the Genomics Era. Rome: FAO; 2009. p 375-378.
104.Liu S, Li X, Wang C, Li X, He Y. Improvement of resistance to rice blast in Zhenshan 97 by molecular markeraided selection. Acta Botanica Sinica 2003; 45(11) 1346-1350.
105.Narayanan NN, Baisakh N, Vera Cruz CM, Gnanamanickam SS, Datta K, Datta SK. Molecular breeding for the development of blast and bacterial blight resistance in rice cv. IR50. Crop Science 2002; 42(6) 2072-2079.
106.Xing J, Jia Y, Correll JC, Lee FN, Cartwright R, Cao M, Yuan L. Analysis of genetic and molecular identity among field isolates of the rice blast fungus with an international differential system, Rep-PCR, and DNA sequencing. Plant diease 2013; 97(4) 491-495.
Open access
