Open access peer-reviewed chapter

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: July 9th, 2013 Reviewed: July 16th, 2013 Published: April 23rd, 2014

DOI: 10.5772/56824

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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 (%)CountryYear
5-10India1960-61
50-60Philippines1963
70-85Philippines1969-70
8Koreamid-70s
14China1980-81
60Thailand1982

Table 1.

Yield losses due to blast.

Source: http://www.knowledgebank.irri.org/ipm/rice-blast.html


1.2. The biology of M. oryzae

The most common symptoms in commercial rice fields induced by M. oryzaecan 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. oryzaeusually 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. oryzaecomplicates the identificationofresistance (R)genes. Physiological races of M. oryzaewere first reported by Sasaki in Japan as early as 1922 [10]. From 1950s to 60s differential rice lines resistant to races of M. oryzaewere identified in Japan, the United States, India, the Philippines, and South Korea. In 1961, 18 physiological races of M. oryzaewere 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. oryzaeraces was initiated in late 1970s. Seven rice varieties, Tebo, Zhenlong13, Sifeng43, Dongnong363, Kanto51, Hejiang18, and Lijiangxintuanheigu (LTH), and 43 isolates of M. oryzaewere used. In 1976, Yamada and his colleagues identified 23 races ofM. oryzaefrom 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. oryzaein China. These blast Rgenes are described in more details in the part II of this chapter. Near-isogenic lines (NILs) were chosen to better identify races ofM. oryzaein a gene-for-gene specific manner. The NILs with indicahigh-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. oryzaewere the most common. Most recently, monogenic lines with 24 major blast Rgenes 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 Rgenes named as Piriculariagenes or Pi-genes. These genes are often specific in preventing infections by strains of M. oryzaethat 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 Rgenes and are extremely important genetic resources that rice breeders can use to improve blast resistance in elite rice varieties.

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2. Mapped blast Rgenes

Blast Rgenes are predicted to play important roles in the frontier of rice defense responses. During interactions between rice and blast pathogens, products of the Rgene can specifically recognize the corresponding elicitors of M. oryzae. Since the Piagene, indentified in 1967 by Kiyosawa as the first blast Rgene from the japonicavariety Aichi Asahi [16], 99 blast Rgenes have been identified; in which 45% were found in japonicacultivars, 51% in indicacultivars, and the rest 4% in wild rice species (Table 2 to 5). Most deployed Rgenes 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 Rgenes 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 Rgenes are summarized in Figure 2 and Table 2 (60 major Rgene) and Table 3 (17 minor Rgene). Among them, three major Rgene clusters have been well characeterized: the Pizlocus on Chromosome 6, the Piklocus on Chromosome 11, and the Pitalocus on Chromosome 12 (Figure 3). More detailed imformation of mapped blast Rgenes can be found at http://www.ricedata.cn/gene/, http://www.shigen.nig.ac.jp/rice/oryzabaseV4/, and http://www.gramene.com.

ChromosomeMajor R genes mapped*Minor R genes mapped*R gene cloned*Total*
12237
273111
30000
41214
52103
6121619
71001
84217
93013
101102
11123823
12152118
Total60172299

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
Rgene
Name ofgermplasmMap position
(cM) >#
MarkersName of pathogenic StrainsRef.
1Pi27(t)*Q1428.4-38.8RM151, RM259CHL0335, CHL0888, CHL0918[17]
1Pitp(t)Tetep114.1RM246IC9[18]
2Pi14(t)MaowanguAmp-1[19]
2Pi16(t)Aus373Amp-1Hoko1, Ina72, TH67-22, Ai75-61[20]
2PiDa(t)Dacca610.8-14.4RM211, RM5529[21]
2Pid1(t)Digu87.5-89.9RM262ZB13[22]
2Pitq-5Teqing150.5-157.5RG520, RZ446bIC-17, IB-49, IE-1, IG-1[23]
2Pig(t)Guangchangzhan142.0-154.1RM166, RM208Ken53-33[24]
2Piy(t)Yanxian No.1153.2-154.1RM3284, RM20897-27-2, Zhong10-8-14[25]
4Pi39(t)*Chubu 111107.4-108.2RM3743, RM5473[26]
5Pi10(t)Tongil88.5-102.8RG13IB46[27]
5Pi23(t)Suweon 36559.3-99.5[28]
6Pi2-1TianjingyeshengdaoAllilic to Pi2/9AP4791, AP4007CHL477, CHL473, P06-6, IC-17, 87-4[29]
6Pi2-2Jefferson58.7RM19817, AP5659-5HN318-2, CHL438, KJ201, ROR1, PO6-6[30]
6Pi8(t)Kasalath74.6-78.2Amp-3Race 447.1[31]
6Pi13(t)*Maowangu74.6-78.2Amp-3[19]
6Pi13(t)*Kasalath67.7-68.5RM2123, RM20155Ken54-04, 95Mu-29, Ina86-137[32]
6Pi22(t)Suweon 36538.4-41.9KJ-201[28]
6Pi26(t)*Gumei 251.0-61.6B10, R674Ca89[33]
6Pi40(t)IR65482-4-136-2-2 O. australiensis54.1-61.6RM527, RM3330KJ105, Ca89, PO6-6, M101-1-29-1, M64-1-3-9[34]
6Pi50(t)Er-Ba-Zhan46.8GDAP51, GDAP1609-3041a, SC0602, SCRB14, HN0102, W06-18a[35]
6Pigm(t)Gumei 465.8C5483, C0428CH109 (ZC13), CH147 (ZB25), CH131 (ZA1)[36]
6PizZenith58.7z4792, z60510, z5765[37]
6Pitq-1Teqing103.0-124.4C236, RG653IC-17, IB-49, IE-1[23]
7Pi17(t)DJ12394.0-104.0Est9[38]
8Pi42(t)Zhe73358.5RM72IE1K[39]
8Pi33(t)IR6445.4RM72, C483Guy11[40]
8Pi55(t)Yuejingsimiao 299.1-102.1RM1345, RM3452CHL688[41]
8PiGD-1(t)Sanhuangzhan 253.7RG1034GD RFDW-I[42]
9Pi3(t)C104PKT,31.3-33.040N23rPO6-6[43]
9Pi15(t)GA2531.3-34.9CRG3, CRG4CHL0416 , Hoku 1[44]
9Pi56(t)Sanhuangzhan 231.3RM24022PO6-6[42]
10PiGD-2(t)Sanhuangzhan 2R16, R14BPO6-6[42]
11Pi18(t)Suweon 365117.9RZ536KI-313[45]
11Pi38(t)Tadukan79.1-88.7RM206, RM21B157[46]
11Pi44(t)Moroberekan91.4-117.9AF349C9240-1[47]
11PiCO39(t)CO3949.1S27126082[48]
11Pilm-2Lemont56.2-117.9R4, RZ536IB54, IG1[23]
11Pi7(t)Moroberekan71.4-84.3RG103, RG16PO6-6[49]
11Pi47(t)Xiangzi 3150104.2-120.1RM206, RM224[50]
11Pi43(t)Zhe733109.5RM1233IE1K[39]
11PiksBengal, M201115.1-117.3RM224, RM1233[51]
11Pikg(t)GA20119.9-120.3[19]
11Piy(t)Yunyin54RM202Sichuang-43[52]
11Pizy(t)Ziyu44102.9RM206ZB13, ZE1[53]
12Pi19(t)Aichi Asahi50.4-51.5RM27937, RM1337CHNO58-3-1, IRBL19-A[54]
12Pita-2Tetep, Pi No.450.4
12Pi6(t)Apura12.2-47.9RG457, RG869[55]
12Pi62(t)Yashiro-mochi12.2-26.0RG9, RZ8164360-R-62[56]
12Pi24(t)*Zhong 15651.5RG241A92-183 (ZC15)[57]
12Pi12(t)Moroberekan47.9RG869[58]
12Pi20(t)IR2451.5-51.8RM1337, RM5364, RM7102BN111[58]
12PiGD-3Sanhuangzhan 255.8RM179GD RFDW-IV[42]
12Pi51(t)TianjingyeshengdaoRM5364, RM27990CHL447, RB5, CHL473, PO6-6[29]
12Pi39(t)*Q1550.4RM27933, RM27940CHL724[59]
12Pi41(t)93-11RM28130CHL1789, CHL347, CHL688[60]
12Pi157(t)Moroberekan49.5-62.2RG341, RG9[61]
12Pi48(t)Xiangzi 3150RM5364, RM7102[50]
12Pitq-6Teqing47.9RG869, RZ397IC-17, IB-49, IE-1, IB-54[23]
12Pih1(t)Hongjiaozhan47.9RG869, RG81ZB1[62]

Table 3.

Summary of major blast Rgenes including their resistance specificity, chromosomal location, map position, and tightly linked DNA markers.

* This Rgene shares the same name with another Rgene.


# 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.


Chr.Name ofRgeneDonorMap position
(cM) >#
DNA MarkersAvirulent race/isolateRef.
1Pi24(t)*Azucena64.4K5CL6[63]
1Pi35(t)Hokkai 188132.0-136.6RM1216, RM1003[64]
2Pir2-3IR64141.7RM263, RM250Race 173[65]
2Pi25(t)*IR64157.9RG520BR26, CH66, CH72[63]
2Pirf2-1(t)O. rufipogon172.3RM206, RM266Race 001[65]
4Pikur1Kuroka86.0[66]
4Pikahei1(t)Kahei108.2RM17496, RM6629[67]
5Pi26(t)*Azucena22.5-24.7RG313PH68[63]
6Pi27(t)*IR6451.9Est-2CH66[63]
8Pi11(t)Zhaiyeqing853.2-84.8BP127A, RZ61718-2, ZH7-2, Zhong10-2-4,[68]
8Pi29(t)IR6469RZ617, RGA-IR86CL6[63]
10Pi28(t)Azucena114.7RZ500PH68[63]
11Pi30(t)IR6459.4-60.4OpZ11-f, RGA-IR14CH66, CH72[63]
11Pi34(t)Chubu3279.1-91.4Z77, Z150-5[69]
11PifSt No. 1119-120[70]
12Pi31(t)IR6444.3O10-800PH68, CD69[63]
12Pi32(t)IR6447.5AF6BR26[63]

Table 4.

Summary of minor blast Rgenes, 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 mappedRgenes on rice chromosomes. The locations ofRgenes 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).

Chr.Rgene clonedDonor and cultivar or line carrying the geneMap position
(cM) >#
MarkersLocus structureProtein typeSubcellular localizationFNPsExpressionRef.
1PitK59, Tjahaja12.2T256MultipleCC-NBS-LRRRepressible[71]
1Pi37St. No1136.1RM302, RM212MultipleNBS-LRRCytoplasmV 239 A, I 247 MConstitutive[72]
1PishShin 2, Norin 22148.7-154.8MultipleCC-NBS-LRRConstitutive[73]
2PibEngkatek, Tohoku IL9, Teqing, Tjinam, BL1154.1RM208MultipleNBS-LRRInducible[74]
4pi21Owarihatamochi58.6P702D03MultipleNBS-LRRCytoplasm[75]
6Pid2Digu (I)65.8SingleReceptor kinaseMembraneI 441 MConstitutive[76]
6Pi9O.minuta,75-1-12758.7MultipleNBS-LRRConstitutive[77]
6Pi2C101A5158.7MultipleNBS-LRRR 838 SConstitutive[78]
6Piz-tTKM, Toride 158.7zt56591MultipleNBS-LRRS 839 RConstitutive[79]
6Pid3Digu65.2-65.8SingleNBS-LRRQ 737 Stop[79]
6Pi25*Gumei 263.2-64.6MultipleCC-NBS-LRR[80]
8Pi36Q61, Kasalath21.6-25.2CRG3SingleNBS-LRRS 590 DConstitutive[81]
9Pi5Tetep, RIL 26031.3-33.076B14r, 40N23rMultipleCC-NBS-LRRCytoplasmPi5-1 is inducible, Pi5-2 is constitutive[82]
11Pi1LAC23, C101LAC112.1-117.9MultipleNBS-LRR[83]
11PikTo-To, Kusabue, Kanto 51, K60, Chugoku 31, Shin 2-1, K2, K3, , Minehikari, GA 20119.9-120.3k8823, k8824,
k3951,
k39512
MultipleCC-NBS-LRRConstitutive[84], [85]
11PikmHokushi,Tsuyuake, IRBLkm-Ts115.1-117.0k2167,
k6441
MultipleNBS-LRRConstitutive[86]
11PikpTetep K60119.9-120.3k3957MultipleCC-NBS-LRRConstitutive[87]
11PikhTetep, K3, Kaybonnet, Lemont, Lebonnet101.9RM224MultipleNBS-LRRInducible[88]
11Pi54rhO. rhizomatis119.9-120.3MultipleCC-NBS-LRRExtracellularInducible[89]
11PiaAichi Asahi36.0Yca72MultipleNBS-LRR[90]
11Pb1Modan, Tsukinohikari,
St NO. 1
85.7-91.4SingleCC-NBS-LRRAge-dependent[91]
12PitaTetep, Katy, Teqing50.4SingleNBS-LRRCytoplasmA 918 SConstitutive[92]

Table 5.

Summary of cloned Rgenes, 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.


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3. Structure and function of blast Rgenes

Among the mapped Rgenes (Table 3 and 4), 22 genes including 20 major and 2 minor Rgenes (Pb1and pi21) have been molecularly characterized (Table 5). Noticeably, Pid2, Pid3, Pi36, Pb1, and Pitaare single copy genes; while others are members of small gene families. A total of eight Rgenes have been identified on chromosome 11, with six at the Piklocus; six Rgenes on chromosome 6, four of which are at the Pizlocus. Most cloned blast Rgenes are adequate in providing complete resistance to strains of M. oryzaethat contain the corresponding avirulence genes. Interestingly, two different members of each of Pi5, Pik, Pikp, Pikm, and Piaare required for complete resistance to some avirulent races.

Figure 4.

Structure of all clonedRgenes. The light green bar represents the length of theRgenes. The highlighted bars represent the different domains of theRgenes.

Similar to other plant Rgenes, all cloned blast Rgenes 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 Pid2and pi21encoding 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 Rproteins 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 Rgenes 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 Pid2and pi21.Among them, Pi1-5, Pik-1, Pikp-1, and Pikm1-TSon chromosome 11 share substantial homology to the Pi9locus on Chromosome 6; whereas, Pi1-6, Pik-2, Pikp-2, and Pikm2-Tare more similar to Pid2and pi21, which are not NBS-LRR Rgenes. Homologous sequences of blast Rgenes 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 blastRgenes. The tree was constructed using protein sequences by software Mega 5.0 NJ method.

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4. Rgene-mediated signaling transduction pathways

It is now commonly accepted that products of Rgenes 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-Pita1by the Pitaprotein was first reported in 2000 [93]. Over a decade later, in 2012, another blast Rprotein, Pik, with similar structure to Pita, was found to directly recognize the corresponding avirulence gene AvrPik[94]. Direct interactions between other blast Rand 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 Rproteins 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 Rproteins. Molecular basis of blast Rgene-mediated signaling has been a subject of intensive investigation worldwide. Abundant genes that may be involved in Rgene-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 Pitamediated signaling was accomplished by treating 20,000 Katy seeds with Pita/Pita2/Piksusing 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 Pitamediated signal transudation [99]. Molecular cloning of Ptr(t)will shed light on the interaction mechanism of Pitaand Ptr(t), and subsequent plant genes involved in defense responses.

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5. The management of blast disease-marker assisted selection

Blast disease has been effectively managed by a combination of fungicides and Rgenes 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 Rgenes 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 Rgenes 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 Rgenes, such as Pi-taand Pi-b, for their introduction into elite rice cultivars using MAS. Markers for Pita, one of the most important Rgenes for blast in the United States, were developed [102]; while, linked markers for 4 blast Rgenes (Pik, Pib, Pita2, and Pii) are effective against eight to ten races of M. oryzaewere identified [103]. Using MAS, Rgenes like Pi1, Pi5, Piz-5, and Pitahave been established in different rice genotypes [82, 100, 104, 105]

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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 Rgene to a specific pathogen race often become susceptible over time due to the emergence of new virulent races. In theory, Rgenes can be found in rice germplasm in different rice production areas. Stacking Rgenes with overlapped resistance spectra can lead to long lasting resistance. Knowledge of genetic identity of contemporary M. oryzaeis crucial for precise deployment of rice cultivars with different Rgenes [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.

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Acknowledgments

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: July 9th, 2013 Reviewed: July 16th, 2013 Published: April 23rd, 2014