Abstract
The genetic control of rice resistance has been extensively studied, but how the resistance mechanism is genetically controlled has received less attention. This study revealed that the rice resistance mechanism toward brown planthopper was genetically controlled by several genes with several mendelian patterns. The tolerance mechanism is controlled by three complementary genes; this is confirmed by QTL analysis, whereas the Antibiosis is controlled by three separate loci on chromosomes 2, 8, and 11. The antixenosis was controlled by polygenic, but detected locus only on chromosome 3, with minor effects.
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Key words: Brown Planthopper, Biotic Stress, Genetic Analysis, Resistance Mechanism
Introduction
Several studies have been conducted to identify genes controlling resistance to brown planthoppers, with not less than 45 genes and QTL found to date (
Li et al. 2024;
Sani Haliru et al. 2020). Several genes have been examined for their resistance mechanisms utilizing phenomics or proteomic approaches (
Muduli et al. 2021), however it remains difficult to uncover loci affecting plant resistance mechanism factors. Plant resistance to pests is frequently composed of several resistance mechanisms that interact or complement one another to promote resistance to the pest. Several studies show that currently antibiosis is the most widely reported mechanism of resistance to brown planthoppers, however, tolerance mechanisms have also been reported to work in several species and varieties (
Sarao et al. 2016). Differences in resistance mechanisms between plant varieties can occur because the plasticity nature of brown planthopper (BPH;
Nilaparvata lugens Stål) populations that increase the variability of BPH population in the world (
Huang et al. 2023).
This study investigates the genetic control of physiological resistance mechanisms that affect rice plants' resistance to brown planthoppers (
Kiswanto et al. 2021;
Kiswanto et al. 2022). Plant resistance to pests can develop because of the plant's response to pests during an attack. Furthermore, the locus governing the resistance mechanism needs to be identified to gain a better understanding of how the genetic control of the resistance mechanism against the brown planthopper works.
Materials and Methods
Plant material and traits
A few 175 F
2:3 lines derived from Balamawee (resistant)×PD601 (susceptible) were used to get sufficient seeds to replicate the phenotyping process. The BPH were acquired from endemic location in Indonesia from 2017 and maintained with TN1 in the greenhouse biotic stress facilities. The antixenosis, antibiosis and tolerance mechanism were studied using the number of nymphs settle (NNS), nymph survival rates (NSR), Functional Plant Loss Index (FPLI) and the Tolerance Index (TI), respectively (
Heinrich, et al. 1985).
Total DNA genomes were extracted from each individual's rice seedling leaves using a slightly modified CTAB technique. Utilizing 71 polymorphic SSR and 2 InDel markers, the PCR result was then examined using agarose gel electrophoresis, and the DNA band pattern was then evaluated. The genetic linkage maps were constructed with ICIMapping 4.2 (
Meng et al. 2015), with LOD score exceeding 2.5 were used to identify the significant QTL on chromosomes (
Li et al. 2024).
Results and Discussion
Gene number controlling resistance mechanism to BPH
The genetic analysis of 175 F2:3 populations revealed that there are two traits with heritability greater than 0.5, namely the NSR and FPLI, indicating that genetic factors have a greater effect than environmental factors. Meanwhile, the heritability for the NNS and TI traits were found to be moderate, at 0.36 and 0.43, respectively. The results further show that the population is normally distributed for NNS and TI, except NSR and FPLI. The test shows that the FPLI and NSR are determined by simple genes, while NNS and TI are controlled by polygenic.
Further analysis revealed that the NSR is regulated by three genes with a 7:57 ratio, and it’s a type of one dominant and two complementary genes with a chi-squared value of 0.58 (X
20.05<5.99). The controls genes of the NSR come from susceptible parent (PD601), as indicated by the distribution of data on the survival rate of nymphs inclined toward susceptible parents (
Fig. 1). Meanwhile, the FPLI showed the inheritance pattern with a ratio of 27R: 37S, as well as its modification 27R: 7MR: 21MS: 7S fit with the distribution pattern. Furthermore, the chi-square value at the 27R:37S ratio compared to the other two ratios indicates that this character is controlled by three complementary genes (
Agbahoungba et al. 2018).
The QTL analysis revealed only three of the four traits studied had significantly identified loci, but each of the three could represent one of the resistance mechanisms. These traits were discovered on chromosomes 2, 3, 4, 8, and 11, with phenotypic explained by QTL (PVE) ranging from 2.31 to 20.40% (
Table 1). The FPLI has three loci, with two having a major effect: qFPLI-2 (20.40%) and qFPLI-3 (15.38%) as suggested by
Collard et al. (2005) a QTL having more than 10% effect is considered as major QTL. Meanwhile, the second locus, qFPLI-1, has a minor effect, with a PVE of 5.11 percent. All these loci have been identified on chromosome 4, with two loci in the long arm (qFPLI-2 and qFPLI-3), and one on the short arm (qFPLI-1). All these loci have additive effects, with Balamawee being the main contributor, as seen by a negative additive value. The NSR (antibiosis) was found and controlled by three loci, one of which, qNSR-1, had a major effect with a PVE value of 10.16 percent. The loci that determine the NSR character is distributed across three chromosomes. This locus’ influence comes mainly from its parent, PD601, with additive effect values of 1.04 and 1.61, respectively. In the antixenosis mechanism, locus identification was carried out on the NNS, resulting in an identified locus on chromosome 3 with a PVE of 6.41%, with additive effects obtained from Balamawee (-0.66). This result shows that the resistance mechanism of rice to BPH is not solely independent on one mechanism only. There is an interaction and combination between resistance mechanism in the plant to overcome the insect attack. Tolerance mechanism showed by Functional Plant Loss Index (FPLI), showing higher contribution in this study, explaining the resistance toward the BPH most likely due to its ability to keep the plant growth normally under BPH attack. Furthermore, closely linked markers to the locus controlling FPLI and NSR can be utilized to select resistance lines toward BPH using Marker assisted selection (MAS) approach in the rice breeding program.
Acknowledgments
This research project was supported by PT BISI International, Tbk. and Faculty of Agriculture of Brawijaya University. The authors also acknowledge the IRRI for providing the resistance donor material in this study.
Fig. 1The distribution of 175 F2:3 lines represent the Resistance Mechanism: A. Number of Nymph Settle on Seedling (Antixenosis); B. Nymph Survival Rate (Antibiosis); C. Functional Plant Loss Index (Tolerance); and D. Tolerance Index (Tolerance).
Table 1Locus controls the resistance mechanism identified in the chromosome of rice
Table 1
|
Locus Code |
Chromosome |
Position (cM) |
Left Marker |
Right Marker |
LOD |
PVE (%) |
Additive |
|
qFPLI-1 |
4 |
36 |
RM8213 |
RM6659 |
2.69 |
5.11 |
-13.20 |
|
qFPLI-2 |
4 |
219 |
Q31 |
RM17007 |
16.66 |
20.40 |
-26.83 |
|
qFPLI-3 |
4 |
233 |
RM17007 |
RM19 |
7.97 |
15.38 |
-19.99 |
|
|
qNSR-1 |
2 |
128 |
RM263 |
RM5404 |
2.74 |
10.16 |
1.04 |
|
qNSR-2 |
8 |
69 |
RM2655 |
RM72 |
3.25 |
2.31 |
1.61 |
|
qNSR-3 |
11 |
16 |
RM286 |
RM552 |
2.86 |
3.97 |
-3.44 |
|
|
qNNS |
3 |
92 |
RM7 |
RM552 |
2.87 |
6.41 |
-0.66 |
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Citations
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