Brown planthopper (BPH), Nilaparvata lugens Stal, is a serious insect pest of rice throughout Asia. Two Indica varieties, ADR52 (from India) and Podiwi A8 (from Sri-Lanka), which previously identified to be resistant to whitebacked planthopper, were also highly resistant to BPH. QTL analysis was conducted to understand the genetic bases of BPH resistance in ADR 52 and Podiwi A8. These varieties were crossed to Taichung 65 (T65), a Japonica variety susceptible to BPH. T65 was used as a female parent whereas the resistant varieties were used as male parents. The F₁ and 81 F₂ of the crosses and the parents were evaluated for antibiosis to BPH by means of nymph mortality. At tillering stage, 5 leaf sheaths of F₂ individuals were infested with 10 second-instar BPH nymphs. The BPH population was collected in Chikugo, Fukuoka Prefecture, Japan in 1989 and was maintained by continuously rearing. Nymph mortality was scored at five days after infestation.

The two resistant parents showed high nymph mortality above 90%. The F₁ of T65/ADR52 was moderately resistant and the frequency distribution in the F₂ was deviated to high nymph mortality. The F₁ of T65/Podiwi A8 was highly resistant with the nymph mortality above 80%. The nymph mortality of the F₂ exhibited a continuous frequency distribution and did not show any discrete segregation.

We constructed two framework maps with 155 and 142 simple sequence repeat (SSR) markers (McCouch et al. 2002) based on the F₂ populations of T65/ADR52 and T65/Podiwi A8, respectively. QTL analyses for antibiosis to BPH were conducted by single factor analysis (SFA) using QGene v3.06 (Nelson 1997) and simple interval mapping (SIM) using QTL Cartographer v1.16 (Basten et al. 2002), with threshold of LOD>=2.0. The same QTLs were detected by using both of the statistical analyses. Therefore, only the results by SIM were shown in Table 1 and Figure 1. In the F₂ population of T65/ADR52, three QTLs affecting antibiosis to BPH were detected on chromosomes 5, 6 and 12. Positive alleles affecting antibiosis to BPH came from ADR52 on chromosomes 6 and 12, and from T65 on chromosome 5. As for Podiwi A8, three QTLs affecting antibiosis to BPH were detected on chromosomes 3, 7 and 12. Alleles from Podiwi A8 contributed to antibiosis to BPH at all the three QTLs.

Three genes for resistance to BPH, Bph1, bph2 and Bph9, are closely linked on chromosome 12 (Hirabayashi and Ogawa 1995, Murata et al. 1998, 2000). Among the two QTLs detected on chromosome 12, the QTL detected in T65/ADR52 was located near Bph1. The

genetic effect showed almost complete dominance, which seemed to be similar to that of Bph1. Another QTL detected in T65/Podiwi A8 was located near bph2 and/or Bph9. The genetic effect of the QTL was additive. Therefore, it is sure that these two QTLs on chromosome 12 are not identical. In the present study, the remaining four QTLs for resistance to BPH were newly detected based on the two F₂ populations compared to the QTLs previously reported (Alam and Cohen 1998, Su et al. 2002). QTLs on chromosomes 6 and 12 controlled BPH antibiosis of ADR52. In the case of Podiwi A8, which seems to be much more resistant than ADR52, the accumulation of three QTLs might affect to antibiosis to BPH. Development of isogenic lines for respective QTLs is necessary to precisely map and characterize the genes for antibiosis to BPH.

References

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Su, C. C., H. Q. Zhai, X. N. Cheng and J. M. Wan, 2002. Detection and analysis of QTLs for resistance to brown planthopper, Nilaparvata lugens (Stal), in rice (Oryza sativa L.), using backcross inbred lines. RGN 19: 88-90.