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Current Advances on Genetic Resistance to Rice Blast Disease

Written By

Xueyan Wang, Seonghee Lee, Jichun Wang, Jianbing Ma, Tracy Bianco and Yulin Jia

Submitted: 09 July 2013 Published: 23 April 2014

DOI: 10.5772/56824

From the Edited Volume

Rice - Germplasm, Genetics and Improvement

Edited by Wengui Yan and Jinsong Bao

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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.

Yield loss (%) Country Year
5-10 India 1960-61
50-60 Philippines 1963
70-85 Philippines 1969-70
8 Korea mid-70s
14 China 1980-81
60 Thailand 1982

Table 1.

Yield losses due to blast.


1.2. The biology of M. oryzae

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 of M. 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 of M. 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 of M. 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.


2. Mapped blast R genes

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,, and

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.

Chr. Name of
R gene
Name of germplasm Map position
(cM) >#
Markers Name of pathogenic Strains Ref.
1 Pi27(t)* Q14 28.4-38.8 RM151, RM259 CHL0335, CHL0888, CHL0918 [17]
1 Pitp(t) Tetep 114.1 RM246 IC9 [18]
2 Pi14(t) Maowangu Amp-1 [19]
2 Pi16(t) Aus373 Amp-1 Hoko1, Ina72, TH67-22, Ai75-61 [20]
2 PiDa(t) Dacca6 10.8-14.4 RM211, RM5529 [21]
2 Pid1(t) Digu 87.5-89.9 RM262 ZB13 [22]
2 Pitq-5 Teqing 150.5-157.5 RG520, RZ446b IC-17, IB-49, IE-1, IG-1 [23]
2 Pig(t) Guangchangzhan 142.0-154.1 RM166, RM208 Ken53-33 [24]
2 Piy(t) Yanxian No.1 153.2-154.1 RM3284, RM208 97-27-2, Zhong10-8-14 [25]
4 Pi39(t)* Chubu 111 107.4-108.2 RM3743, RM5473 [26]
5 Pi10(t) Tongil 88.5-102.8 RG13 IB46 [27]
5 Pi23(t) Suweon 365 59.3-99.5 [28]
6 Pi2-1 Tianjingyeshengdao Allilic to Pi2/9 AP4791, AP4007 CHL477, CHL473, P06-6, IC-17, 87-4 [29]
6 Pi2-2 Jefferson 58.7 RM19817, AP5659-5 HN318-2, CHL438, KJ201, ROR1, PO6-6 [30]
6 Pi8(t) Kasalath 74.6-78.2 Amp-3 Race 447.1 [31]
6 Pi13(t)* Maowangu 74.6-78.2 Amp-3 [19]
6 Pi13(t)* Kasalath 67.7-68.5 RM2123, RM20155 Ken54-04, 95Mu-29, Ina86-137 [32]
6 Pi22(t) Suweon 365 38.4-41.9 KJ-201 [28]
6 Pi26(t)* Gumei 2 51.0-61.6 B10, R674 Ca89 [33]
6 Pi40(t) IR65482-4-136-2-2 O. australiensis 54.1-61.6 RM527, RM3330 KJ105, Ca89, PO6-6, M101-1-29-1, M64-1-3-9 [34]
6 Pi50(t) Er-Ba-Zhan 46.8 GDAP51, GDAP16 09-3041a, SC0602, SCRB14, HN0102, W06-18a [35]
6 Pigm(t) Gumei 4 65.8 C5483, C0428 CH109 (ZC13), CH147 (ZB25), CH131 (ZA1) [36]
6 Piz Zenith 58.7 z4792, z60510, z5765 [37]
6 Pitq-1 Teqing 103.0-124.4 C236, RG653 IC-17, IB-49, IE-1 [23]
7 Pi17(t) DJ123 94.0-104.0 Est9 [38]
8 Pi42(t) Zhe733 58.5 RM72 IE1K [39]
8 Pi33(t) IR64 45.4 RM72, C483 Guy11 [40]
8 Pi55(t) Yuejingsimiao 2 99.1-102.1 RM1345, RM3452 CHL688 [41]
8 PiGD-1(t) Sanhuangzhan 2 53.7 RG1034 GD RFDW-I [42]
9 Pi3(t) C104PKT, 31.3-33.0 40N23r PO6-6 [43]
9 Pi15(t) GA25 31.3-34.9 CRG3, CRG4 CHL0416 , Hoku 1 [44]
9 Pi56(t) Sanhuangzhan 2 31.3 RM24022 PO6-6 [42]
10 PiGD-2(t) Sanhuangzhan 2 R16, R14B PO6-6 [42]
11 Pi18(t) Suweon 365 117.9 RZ536 KI-313 [45]
11 Pi38(t) Tadukan 79.1-88.7 RM206, RM21 B157 [46]
11 Pi44(t) Moroberekan 91.4-117.9 AF349 C9240-1 [47]
11 PiCO39(t) CO39 49.1 S2712 6082 [48]
11 Pilm-2 Lemont 56.2-117.9 R4, RZ536 IB54, IG1 [23]
11 Pi7(t) Moroberekan 71.4-84.3 RG103, RG16 PO6-6 [49]
11 Pi47(t) Xiangzi 3150 104.2-120.1 RM206, RM224 [50]
11 Pi43(t) Zhe733 109.5 RM1233 IE1K [39]
11 Piks Bengal, M201 115.1-117.3 RM224, RM1233 [51]
11 Pikg(t) GA20 119.9-120.3 [19]
11 Piy(t) Yunyin 54 RM202 Sichuang-43 [52]
11 Pizy(t) Ziyu44 102.9 RM206 ZB13, ZE1 [53]
12 Pi19(t) Aichi Asahi 50.4-51.5 RM27937, RM1337 CHNO58-3-1, IRBL19-A [54]
12 Pita-2 Tetep, Pi No.4 50.4
12 Pi6(t) Apura 12.2-47.9 RG457, RG869 [55]
12 Pi62(t) Yashiro-mochi 12.2-26.0 RG9, RZ816 4360-R-62 [56]
12 Pi24(t)* Zhong 156 51.5 RG241A 92-183 (ZC15) [57]
12 Pi12(t) Moroberekan 47.9 RG869 [58]
12 Pi20(t) IR24 51.5-51.8 RM1337, RM5364, RM7102 BN111 [58]
12 PiGD-3 Sanhuangzhan 2 55.8 RM179 GD RFDW-IV [42]
12 Pi51(t) Tianjingyeshengdao RM5364, RM27990 CHL447, RB5, CHL473, PO6-6 [29]
12 Pi39(t)* Q15 50.4 RM27933, RM27940 CHL724 [59]
12 Pi41(t) 93-11 RM28130 CHL1789, CHL347, CHL688 [60]
12 Pi157(t) Moroberekan 49.5-62.2 RG341, RG9 [61]
12 Pi48(t) Xiangzi 3150 RM5364, RM7102 [50]
12 Pitq-6 Teqing 47.9 RG869, RZ397 IC-17, IB-49, IE-1, IB-54 [23]
12 Pih1(t) Hongjiaozhan 47.9 RG869, RG81 ZB1 [62]

Table 3.

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

‡ Information is known, but has not been published.

Chr. Name of R gene Donor Map position
(cM) >#
DNA Markers Avirulent race/isolate Ref.
1 Pi24(t)* Azucena 64.4 K5 CL6 [63]
1 Pi35(t) Hokkai 188 132.0-136.6 RM1216, RM1003 [64]
2 Pir2-3 IR64 141.7 RM263, RM250 Race 173 [65]
2 Pi25(t)* IR64 157.9 RG520 BR26, CH66, CH72 [63]
2 Pirf2-1(t) O. rufipogon 172.3 RM206, RM266 Race 001 [65]
4 Pikur1 Kuroka 86.0 [66]
4 Pikahei1(t) Kahei 108.2 RM17496, RM6629 [67]
5 Pi26(t)* Azucena 22.5-24.7 RG313 PH68 [63]
6 Pi27(t)* IR64 51.9 Est-2 CH66 [63]
8 Pi11(t) Zhaiyeqing8 53.2-84.8 BP127A, RZ617 18-2, ZH7-2, Zhong10-2-4, [68]
8 Pi29(t) IR64 69 RZ617, RGA-IR86 CL6 [63]
10 Pi28(t) Azucena 114.7 RZ500 PH68 [63]
11 Pi30(t) IR64 59.4-60.4 OpZ11-f, RGA-IR14 CH66, CH72 [63]
11 Pi34(t) Chubu32 79.1-91.4 Z77, Z150-5 [69]
11 Pif St No. 1 119-120 [70]
12 Pi31(t) IR64 44.3 O10-800 PH68, CD69 [63]
12 Pi32(t) IR64 47.5 AF6 BR26 [63]

Table 4.

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

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:

Chr. R gene cloned Donor and cultivar or line carrying the gene Map position
(cM) >#
Markers Locus structure Protein type Subcellular localization FNPs Expression Ref.
1 Pit K59, Tjahaja 12.2 T256 Multiple CC-NBS-LRR Repressible [71]
1 Pi37 St. No1 136.1 RM302, RM212 Multiple NBS-LRR Cytoplasm V 239 A, I 247 M Constitutive [72]
1 Pish Shin 2, Norin 22 148.7-154.8 Multiple CC-NBS-LRR Constitutive [73]
2 Pib Engkatek, Tohoku IL9, Teqing, Tjinam, BL1 154.1 RM208 Multiple NBS-LRR Inducible [74]
4 pi21 Owarihatamochi 58.6 P702D03 Multiple NBS-LRR Cytoplasm [75]
6 Pid2 Digu (I) 65.8 Single Receptor kinase Membrane I 441 M Constitutive [76]
6 Pi9 O.minuta, 75-1-127 58.7 Multiple NBS-LRR Constitutive [77]
6 Pi2 C101A51 58.7 Multiple NBS-LRR R 838 S Constitutive [78]
6 Piz-t TKM, Toride 1 58.7 zt56591 Multiple NBS-LRR S 839 R Constitutive [79]
6 Pid3 Digu 65.2-65.8 Single NBS-LRR Q 737 Stop [79]
6 Pi25* Gumei 2 63.2-64.6 Multiple CC-NBS-LRR [80]
8 Pi36 Q61, Kasalath 21.6-25.2 CRG3 Single NBS-LRR S 590 D Constitutive [81]
9 Pi5 Tetep, RIL 260 31.3-33.0 76B14r, 40N23r Multiple CC-NBS-LRR Cytoplasm Pi5-1 is inducible, Pi5-2 is constitutive [82]
11 Pi1 LAC23, C101LAC 112.1-117.9 Multiple NBS-LRR [83]
11 Pik To-To, Kusabue, Kanto 51, K60, Chugoku 31, Shin 2-1, K2, K3, , Minehikari, GA 20 119.9-120.3 k8823, k8824,
Multiple CC-NBS-LRR Constitutive [84], [85]
11 Pikm Hokushi,Tsuyuake, IRBLkm-Ts 115.1-117.0 k2167,
Multiple NBS-LRR Constitutive [86]
11 Pikp Tetep K60 119.9-120.3 k3957 Multiple CC-NBS-LRR Constitutive [87]
11 Pikh Tetep, K3, Kaybonnet, Lemont, Lebonnet 101.9 RM224 Multiple NBS-LRR Inducible [88]
11 Pi54rh O. rhizomatis 119.9-120.3 Multiple CC-NBS-LRR Extracellular Inducible [89]
11 Pia Aichi Asahi 36.0 Yca72 Multiple NBS-LRR [90]
11 Pb1 Modan, Tsukinohikari,
St NO. 1
85.7-91.4 Single CC-NBS-LRR Age-dependent [91]
12 Pita Tetep, Katy, Teqing 50.4 Single NBS-LRR Cytoplasm A 918 S Constitutive [92]

Table 5.

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


3. Structure and function of blast R genes

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]


6. Future prospects

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.


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Written By

Xueyan Wang, Seonghee Lee, Jichun Wang, Jianbing Ma, Tracy Bianco and Yulin Jia

Submitted: 09 July 2013 Published: 23 April 2014