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Published online 19 March 2008
Published in Crop Sci 48:480-486 (2008)
© 2008 Crop Science Society of America
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Characterization of a Putative Rice Mutant for Reaction to Rice Tungro Disease

N. S. Zenna, P. Q. Cabauatan, M. Baraoidan, H. Leung and I.-R. Choi*

International Rice Research Institute (IRRI), Plant Breeding, Genetics, and Biotechnology Division, DAPO Box 7777, Metro Manila, Philippines

* Corresponding author (ichoi{at}cgiar.org).


   ABSTRACT
TOP
 NOTES
 ABSTRACT
INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Artificial mutations may induce traits that are scarce among natural germplasm sources. This study was conducted to characterize a rice line derived from variety IR64 showing resistance to rice tungro disease (RTD). Approximately 24,000 lines derived from IR64 seeds treated with mutagens were evaluated for reaction to RTD. One of the lines, M4D6 83-1 (MD83), showed enhanced resistance to RTD. MD83 was resistant to rice tungro spherical virus (RTSV) and the virus vector, green leafhopper (GLH; Nephotettix virescens Distant). MD83 was crossed with susceptible varieties IR64 and Taichung Native 1. All F1 plants were susceptible to RTSV, whereas F2 and F3 progenies segregated into resistant and susceptible phenotypes in a 1:3 ratio, indicating that the resistance is controlled by a single recessive locus. Most of the F3 lines resistant to RTSV were also GLH resistant, suggesting that the resistance to RTSV and GLH was governed by the same locus. It has been difficult to prove whether the genotype MD83 was a product of a mutation event or was represented in the variety IR64 at a very low frequency.

Abbreviations: DAI, days after inoculation • ELISA, enzyme-linked immunosorbent assay • GLH, green leafhopper • RTBV, rice tungro bacilliform virus • RTD, rice tungro disease • RTSV, rice tungro spherical virus • SSR, simple sequence repeat • TN1, Taichung Native 1


   INTRODUCTION
TOP
 NOTES
 ABSTRACT
 INTRODUCTION
MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
RICE TUNGRO DISEASE (RTD) is among the most important viral diseases of rice in tropical Asia. Rivera and Ou (1965) demonstrated the viral nature of RTD and showed that it can be transmitted only by leafhoppers, mainly the green leafhopper (GLH; Nephotettix virescens Distant) (Hibino, 1983). Rice tungro disease is caused by a composite of viruses, rice tungro bacilliform virus (RTBV) and rice tungro spherical virus (RTSV) (Hibino, 1983). Plants infected simultaneously with RTSV and RTBV show symptoms such as yellowing and reddening of leaves, stunting, and often severe necrosis (Hibino, 1983). Rice tungro disease can devastate thousands of hectares of rice in a single outbreak. Though major outbreaks are infrequent, RTD can wipe out small farms in irrigated rice-producing areas where the disease is endemic (Azzam and Chancellor, 2002).

Among more than 40,000 germplasm accessions evaluated for reactions to RTD, a small proportion of accessions was found to be tolerant to resistant (Hibino et al., 1990), but only a few of them were genetically characterized. It was reported that RTSV resistance in one cultivar, Utri Merah, was determined by two recessive genes, tsv1 and tsv2, and that tsv1 was also responsible for RTSV resistance in cultivars Utri Rajapan and Pankhari 203 (Ebron et al., 1994; Shahjahan et al., 1991). Sebastian et al. (1995) showed that resistance to GLH and RTSV in cultivar ARC11554 was governed by dominant loci located 5.5 cM apart on chromosome 4.

Mutagenesis that gives a desirable phenotype without disturbing the basic genotype has been an attractive approach for plant breeders (Mikaelsen 1979). The introduction of mutations could shorten the breeding scheme compared with conventional methods, in which certain genes have to be incorporated from another genetic background through a series of backcrosses. Maluszynski et al. (2000) reported that more than 2200 crop varieties developed by mutations had been officially released, including 434 rice varieties such as Nipponbare, Ptb 10, Ptb 28, Taichung Native 1 (TN1), and Taipei 309. Plant height, flowering and maturity time, and pest and disease resistance are among the traits that were altered in rice varieties by mutagenesis (Mikaelsen, 1979).

A large collection of mutants was produced from IR64, an indica rice variety with good agronomic performance in Asia (Leung et al., 2001). The mutants were produced by chemical treatments (diepoxybutane and ethyl methanesulphonate) or irradiation (fast neutron or gamma rays). The mutants were evaluated for various biotic and abiotic stresses to identify those with promising traits. For instance, a few mutant lines with gain- and loss-of-resistance phenotypes for blast (Pyricularia oryzae Cavara [anamorph]; Magnaporthe oryzae B. Couch [teleomorph]), bacterial blight [Xanthomonas oryzae pv. oryzae (Ishiyama) Swings et al.], and tungro virus were identified from forward genetic screens (Wu et al., 2005).

The objectives of this study were (i) to define the biological and genetic characteristics of the resistance to RTD observed in one of the mutants, M4D6 83-1, by evaluating the levels of resistance to RTSV, RTBV, and the insect vector, and (ii) to determine the inheritance of resistance to RTD and GLH.


   MATERIALS AND METHODS
TOP
 NOTES
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
RESULTS
 DISCUSSION
 REFERENCES
 
Production of IR64 Mutants
The production of the IR64 mutant collection was described in detail by Wu et al. (2005). Briefly, chemically induced IR64 mutants were produced by soaking IR64-HD175 seeds in an aqueous solution of 0.004% or 0.006% diepoxybutane in a shaker at 30°C for 13 h with gentle shaking. Irradiation-induced mutants were produced by exposing IR64-21 seeds to doses of 250 GY for gamma ray and 33 GY for fast neutron.

Evaluation for Tungro Virus Infection
About 24,000 M3 or M4 lines were screened for altered reactions to RTD by the mass evaluation method (Azzam et al., 2000). For each line, 20 6-d-old seedlings were inoculated with RTBV or RTSV viruliferous GLH. Infection of plants with tungro viruses was determined at 3 wk after inoculation by enzyme-linked immunosorbent assay (ELISA) (Bajet et al., 1985). The reaction (resistance or susceptibility) of each line to tungro viruses was evaluated based on the rate of infection with RTBV or RTSV. Infection rate for each line was computed as (the number of infected plants/the number of inoculated plants) x 100 (%).

The reaction of line M4D6 83-1 (MD83, hereafter) to RTD was confirmed in the plants inoculated by the forced-tube method (Azzam et al., 2000). Thirty seedlings of MD83, IR64, TN1 (susceptible to GLH), and IR62 (GLH-resistant variety) were inoculated with one, three, and five viruliferous GLH per plant. The experiment was performed in a complete randomized design with six replications. The mean rates of infection were compared using the least significant difference (LSD) test.

To examine temporal changes in RTSV and RTBV infections, 20 6-d-old seedlings of MD83, IR64, and TN1 were inoculated by the forced-tube method. Leaves from 20 plants per variety were collected at 0, 3, 7, 10, 17, 24, and 31 d after inoculation (DAI) to examine virus infection by ELISA. Temporal changes in RTBV infection were also evaluated in plants inoculated by the Agrobacterium-mediated method (agroinoculation; Sta Cruz et al., 1999). The respective experiments were performed in a complete randomized design with four replications.

Evaluation for GLH Resistance
A host choice test was conducted by the mass infestation of 6-d-old seedlings with virus-free GLH at the rate of five insects per seedling. The number of insects alighted on each seedling was recorded at 0.5, 2, 4, 6, and 8 h after the introduction of GLH. A GLH infestation test was performed as described by Heinrichs et al. (1985). Twenty seedlings per variety were tested in a complete randomized design with four replications. Plants were kept infested with GLH until 50% of the TN1 plants died. Symptom severity score (IRRI, 1996), plant height reduction due to insect feeding, and dry biomass loss relative to the healthy check were examined. The results were analyzed by LSD tests.

Genetic Characterization of RTD Resistance in MD83
Progenies (F1, F2, and F3) were produced from TN1/MD83, IR64/MD83, and TN1/IR64 crosses and the corresponding reciprocal crosses. Thirty seedlings of F1 plants and their parents, 240 F2 seedlings, and 204 F3 lines (30 seedlings per line) from different crosses were inoculated with three RTSV-viruliferous GLH per seedling by the forced-tube method. Leaves were collected from each plant at 21 DAI to examine RTSV infection by ELISA. The experiments were performed in a complete randomized design. The segregation pattern of resistance from MD83 was determined by {chi}2 tests based on the numbers of infected (ELISA value ≥ 0.1) and noninfected plants (ELISA value < 0.1) for F2 populations, and by infection rate classifications (see Results) for F3 lines.

Segregation of GLH resistance in MD83-derived segregating populations was also examined using the same F3 lines that were tested for RTSV resistance. Thirty seedlings per line were mass infested with five virus-free GLH per seedling. The levels of GLH resistance were evaluated with the average height and biomass losses due to infestation.

A genetic polymorphism survey was conducted for IR64, MD83, and TN1 using 540 simple sequence repeat (SSR) markers to confirm that MD83 was derived from IR64. Additional genetic background validation of MD83 was conducted by comparing the genotype of MD83 with that of other GLH- and tungro virus–resistant varieties, such as IR62, IR36, PTB18, ARC11554, Matatag 9, and Aday Selection, using 63 randomly selected SSR markers. A dendrogram indicating the relatedness among the varieties was constructed using the TREE program of NTSYS-pc (Rohlf, 1998).


   RESULTS
TOP
 NOTES
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
DISCUSSION
 REFERENCES
 
Evaluation of MD83 for RTD Resistance
From screening of 24,000 lines, three lines were identified that showed altered reactions to RTD by the mass evaluation. These were MD83 (original designation M4D6 83-1) showing milder symptoms than IR64 by the mass inoculation; M4D6 245-9-4-2 showing severer symptoms; and M4GR 3680 with a hypersensitive (necrosis) reaction. Only MD83 was subjected to further characterization in this study. By the mass evaluation, the infection rate of RTSV in MD83 was about 10%, while that of RTBV was more than 80%.

Further examination of MD83 showed that the infection rate in MD83 was similar to that in IR62 but significantly different from that in IR64 and TN1 (Table 1 ). Although there was an abrupt increase in infection rate for both MD83 (53.3%) and IR62 (56.7%) when inoculated with five insects per seedling, the infection rate in MD83 was still significantly lower than that in TN1 and IR64. In the observation for temporal changes in infection rates, IR64 and TN1 exhibited more than 50% RTSV infection as early as 7 DAI and reached a maximum infection rate of about 70 and 95%, respectively, during the fourth week after inoculation. In contrast, the infection rates in MD83 remained approximately 20% throughout the observation period (Fig. 1 ).


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  		Table 1. Infection rates of rice tungro spherical virus (RTSV) in TN1, IR64, MD83, and IR62 using the forced-tube inoculation technique.

 

Figure 1
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  		Figure 1. Temporal changes in rice tungro spherical virus (RTSV) infection rate (%) in MD83, IR64, and Taichung Native 1 (TN1) by the forced-tube inoculation method. Vertical lines indicate the standard error for RTSV infection rates at the respective time points. Means and standard errors were based on four replicated experiments.

 
No drastic differences in RTBV infection rates among IR64, TN1, and MD83 were observed. The infection rates in plants agroinoculated with RTBV reached a maximum at 17 to 24 DAI, and then gradually declined (Fig. 2A ). The RTBV infection rates in plants inoculated with RTBV and RTSV viruliferous GLH reached a maximum at 10 to 17 DAI, and remained at a similar level in IR64 and TN1 for more than 30 DAI (Fig. 2B). Although MD83 was infected with RTSV and RTBV, infected plants of MD83 showed milder symptoms than IR64, suggesting that MD83 has an ability to suppress tungro symptom expression (Fig. 3 ).


Figure 2
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  		Figure 2. Temporal changes in rice tungro bacilliform virus (RTBV) infection rate (%) in MD83, IR64, and Taichung Native 1 (TN1) by (A) agroinoculation and (B) insect transmission methods. Vertical lines indicate the standard error for RTBV infection rates at the respective time points. Means and standard errors were based on four replicated experiments.

 

Figure 3
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  		Figure 3. Reactions of a highly susceptible mutant (M4D6 245-9-4-2), resistant mutant (MD83), and IR64 to simultaneous infection with rice tungro spherical virus (RTSV) and rice tungro bacilliform virus (RTBV) by the insect transmission method. Plants were confirmed infected with both RTSV and RTBV by enzyme-linked immunosorbent assay (ELISA).

 
Resistance of MD83 Against GLH
A larger number of GLH settled on TN1 and IR64 than on IR62 and MD83, indicating the preference of GLH for TN1, followed by IR64 over IR62 and MD83 (Fig. 4 ). Consequently, MD83 and IR62 were the least damaged by GLH, registering a low symptom severity score of 3, whereas IR64 and TN1 were severely damaged, with symptom scores of 7 and 9, respectively. The average height reduction due to GLH infestation was about 60% for TN1 and IR64 and <40% for MD83 and IR62 (Table 2 ). As a result, TN1 and IR64 had 60% or more reduction in their dry biomass, whereas MD83 and IR62 had <40% biomass reduction due to the infestation (Table 2). Collectively, these results show that MD83 has a significant level of GLH resistance (antixenosis) comparable to that of the GLH-resistant variety IR62.


Figure 4
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  		Figure 4. Temporal changes in the numbers of green leafhopper (GLH) alighted on Taichung Native 1 (TN1), IR64, MD83, and IR62 during the host choice test. Vertical lines indicate the standard error for the numbers of GLH per plant among 20 plants at the respective time points. Means and standard errors were based on four replicated experiments.

 

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  		Table 2. Percent dry biomass and height reduction in plants infested with virus-free green leafhopper (GLH) relative to those of healthy controls.

 
Genetic Characterization of MD83 and Progenies for RTD
Evaluation for RTBV infection was excluded in further genetic analysis of RTD resistance in MD83 since considerable differences in RTBV infection rate were not observed among MD83, IR64, and TN1. All F1 plants from the crosses TN1/MD83, IR64/MD83, and TN1/IR64, and the corresponding reciprocal crosses were found to be susceptible to RTSV based on ELISA. The evaluation of 240 F2 genotypes of TN1/MD83 and IR64/MD83 crosses against RTSV showed a Mendelian segregation ratio of one resistant (not infected with RTSV) to three susceptible (infected with RTSV), suggesting that the resistance phenotype is inherited as a recessive trait with a major effect on RTD resistance (Table 3 ).


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  		Table 3. Chi-square tests for 3:1 segregation pattern for rice tungro spherical virus (RTSV) resistance in F2 and F3 generations derived from TN1/MD83, IR64/MD83, and TN1/IR64.

 
The criterion for the resistance in F2:3 lines was established based on the infection rate of MD83. The results of ELISA for RTSV infection indicated that the rates of infection in MD83 by the forced-tube method were <30%. For the evaluations by two classifications, lines showing 0 to 30% infection rates were classified as resistant, whereas those between 31 and 100% were considered susceptible. Based on this criterion, the 204 F2:3 lines from TN1/MD83 and IR64/MD83 segregated in a one resistant to three susceptible ratio for reaction to RTSV, consistent with the inheritance pattern of a recessive gene (Table 3). We further tested the segregation using an evaluation scheme that considered lines with 31 to 61% infection rates as intermediate. When the F3 lines were classified into three classes—resistant, intermediate, and susceptible—the {chi}2 test showed that the segregation patterns for TN1/MD83 ({chi}2 = 0.705 at P = 0.7) and IR64/MD83 ({chi}2 = 1.26 at P = 0.5) populations were consistent with the expected Mendelian ratio of 1:2:1. These results suggested that RTSV resistance was controlled by a single recessive locus in both TN1/MD83 and IR64/MD83 populations. The F2 and F3 progenies of the TN1/IR64 cross, however, did not fit the 3:1 segregation pattern (Table 3) as both parents are susceptible to RTSV, and only IR64 exhibited partial resistance to GLH.

Based on the evaluation of the F3 lines for the mean dry biomass and height reduction by GLH infestation, 38% of the 204 F3 lines produced from TN1/MD83 were resistant to GLH. Among the RTSV-resistant lines, 95% of them were also resistant to GLH (Fig. 5A ). In F3 lines from IR64/MD83, 41% of them were resistant to GLH (Fig. 5B) and 76% of the RTSV-resistant lines were also resistant to GLH. Among the F3 lines derived from the control cross TN1/IR64, 21% of them had GLH resistance and 15% of the GLH-resistant lines appeared to be resistant to RTSV. Segregation patterns of the control cross suggested that some resistance factors with a minor effect could be segregating, or it reflected the imperfect nature of screening.


Figure 5
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  		Figure 5. (A) Percentages of F3 lines derived from Taichung Native 1 (TN1)/MD83 that showed resistance to rice tungro spherical virus (RTSV) (horizontal stripes), RTSV and green leafhopper (GLH) (checkered lines), and GLH (vertical stripes). (B) Percentages of F3 lines derived from IR64/MD83 that showed resistance to rice tungro spherical virus (RTSV) (horizontal stripes), RTSV and GLH (checkered lines), and GLH (horizontal stripes).

 
The genetic polymorphism survey with 540 SSR markers indicated 4% differences between MD83 and IR64 and 17% between MD83 and TN1. The result of genetic background validation with 63 SSR markers showed 84% similarity between MD83 and IR64 and 79% between MD83 and IR62. The rest of the varieties showed <70% similarity with MD83 (Fig. 6 ).


Figure 6
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  		Figure 6. Phylogenetic tree showing relatedness between eight rice varieties and mutant line MD83. The similarity matrix was generated according to the coefficient obtained through the unweighted pair group method with arithmetic mean (UPGMA) function of NTSYS-pc software.

 

   DISCUSSION
TOP
 NOTES
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
REFERENCES
 
Out of more than 24,000 IR64 mutant lines evaluated for reactions to RTD, one line, MD83, was identified to show enhanced resistance to RTSV and GLH. If we consider the other two mutants with an altered response to RTD, we have a recovery rate of 3/24,000 (0.01%), which is about an order of magnitude less than the recovery of mutations in other traits (Wu et al., 2005). For example, the recovery of mutations with altered response to salinity stress was 0.16% (Nakhoda et al., 2006). For disease response, we obtained gain- or loss-of-resistance to rice blast at about 0.4% (unpublished data).

The rates of infection with RTSV in MD83 were noticeably lower than in IR64 in both mass and forced-tube inoculation tests. Inoculation of RTBV in MD83 by Agrobacterium- and GLH-mediated transmission resulted in a high level of infection, indicating that the resistance was not effective against RTBV. However, less severe tungro symptoms were observed in MD83 than in IR64 (Fig. 3), probably due to the tolerance of MD83 to suppress the disease symptom.

At different levels of GLH-mediated inoculum, MD83 consistently exhibited lower infection rates with RTSV than IR64. A significant increase in the infection rate was observed because of high inoculum pressure (i.e., five viruliferous GLH per plant) (Table 1), suggesting that the optimum inoculum level to differentiate contrasting phenotypes for RTSV infection for practical screening purposes should be about three GLH per seedling.

Temporal analyses of RTBV and RTSV infection at different seedling ages (Fig. 1 and 2) showed that MD83 can be infected with both RTBV and RTSV, and that RTBV can infect MD83 with relatively high efficiency. However, the accumulation rates for the two viruses were different, as the maximum infection rates with RTBV in plants appeared about a week earlier than those with RTSV. These results imply that sampling for the respective viruses should be conducted separately to determine actual infection rates.

Results from the mass infestation experiment for the evaluation of GLH resistance showed the evident preference of GLH for TN1 and IR64 over MD83, was probably due to the antixenosis characteristics of MD83. The difference in the reduction ratios in height and dry biomass caused by GLH infestation indicates that MD83 has a significant level of antixenosis to GLH compared with TN1 and IR64. The antixenosis level of MD83 against GLH appeared to be comparable to that of GLH-resistant variety IR62.

Genetic analysis of RTSV resistance in MD83 indicated the involvement of a single recessive locus. Previous studies on induced mutations for many traits indicated the involvement of recessive genes (Mikaelsen, 1979). Recessive resistance to RTD in rice cultivars such as Utri Merah was also characterized previously (Ebron et al., 1994). Recessive resistance to viruses is thought to be a form of passive incompatibility resulting from the lack of a specific host factor required by viruses to complete their infection cycle (Diaz-Pendon et al., 2004). Genes indispensable for the RTSV infection cycle in MD83 might have been disabled without affecting normal growth of the plant.

Concurrent analysis of resistance to GLH and RTSV in the F3 lines derived from the crosses TN1/MD83 and IR64/MD83 demonstrated that a majority of the RTSV-resistant lines were also resistant to GLH, but nearly half of the GLH-resistant lines were not RTSV resistant. The virus resistance exhibited by MD83 and its progenies could be mainly due to the inhibition of RTSV replication at an early stage, although GLH resistance in MD83 may have also contributed to the apparent resistance to RTD. Sebastian et al. (1995) observed a tight linkage between GLH and RTSV resistance in cultivar ARC11544. Similarly, RTSV and GLH resistance could be tightly linked in MD83. Alternatively, RTSV and GLH resistance could be governed by the same gene, as observed with the Mi gene in tomato (Solanum lycopersicum L.), which confers resistance against aphids and nematodes, organisms from different phyla (Rossi et al., 1998). However, if the same locus is conferring resistance to both RTSV and GLH, why was perfect cosegregation not observed? One possibility is that resistance to GLH could be influenced by other unknown modifying factors present in TN1 and IR64. For example, it is known that IR64 has some level of resistance to GLH, though the exact genetic loci or quantitative trait loci have not been mapped. Segregation of these factors may skew the reaction of GLH.

Although genotyping with SSR markers showed 4% polymorphism between IR64 and MD83, we believe that this level of variation falls within the range of residual heterogeneity found in IR64 seed stock as reported by Wu et al. (2007). Out of 94 plants genotyped with 45 SSR markers, Wu et al. (2007) detected a predominate type at 70% frequency and nine subtypes with frequencies of 1 to 8%. The authors were able to trace the variation back to heterozygous loci maintained in the seed stock. Thus, the polymorphism found between MD83 and IR64 could be a reflection of the existing variation in IR64 seeds used for mutagenesis. Conclusive evidence of the relatedness between MD83 and IR64 came from a comparison with genotypes of other insect- and/or virus-resistant varieties. All genotypes, except IR62, are found to be dissimilar to MD83, indicating that MD83 is unlikely to be a contaminant. The similarity between MD83 and IR62 could be explained by the common pedigrees shared between IR62 and IR64 (Khush and Virk, 2005). Although the genotyping data suggest that MD83 was derived from IR64, we could not unequivocally determine whether the genotypic difference between IR64 and MD83 is due to induced mutation or to existing natural variation within IR64. Nonetheless, our results show that through intensive screening and characterization, it is possible to detect rare genotypes within a crop variety.

The apparent resistance to RTD in MD83 may result from a combined effect between the suppression of symptom development and enhancement of GLH/RTSV resistance. Since MD83 does not appear to have obvious pleiotropic effects on other agronomic traits, it can be a potential source of resistance to RTD. Furthermore, the enhanced resistance in MD83 provides an entry point to investigate the mechanisms of viral and insect resistance in rice. A comparison of MD83 and IR64 (or a susceptible segregant) essentially presents an isogenic contrast that could facilitate the molecular characterization of the resistance locus in MD83 and eventual use of this resistance in breeding for tungro virus resistance.


   ACKNOWLEDGMENTS
 
The authors would like to thank the Swiss Agency for Development and Cooperation and the Rural Development Administration of Korea for financial support, and the staff of the virology group at IRRI for generous assistance.


   NOTES
TOP
 NOTES
ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
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Received for publication March 6, 2007.


   REFERENCES
TOP
 NOTES
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 





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