Genes for Resistance to Russian Wheat Aphid in Two New Wheat Lines

R.S. Pathak¹, J.N. Malinga², M.G. Kinyua², J.K. Wanjama³ and A.W. Kamau¹

¹Deptartment of Agronomy, Egerton University, P.O. Box 536, Njoro, Kenya Email:ramspathak@yahoo.com ²National Plant Breeding Research Centre, P.O. Njoro, Kenya³Ministry of Agriculture and Rural Development, P.O. Box 30028, Nairobi, Kenya

Abstract

The Russian wheat aphid (RWA), Diuraphis noxia (Mordvilko), is a recent pest of wheat (Triticum aestivum L.) in Kenya and it causes severe yield losses up to 90 percent. The most effective, economical and environmentally safe strategy for controlling RWA is the use of genetic resistance. The study was conducted to determine the genetic model of gene(s) conferring resistance to RWA in two Turkish wheat lines, KRWAPC-8 and KRWAPC-16. The resistant lines were crossed with the susceptible commercial wheat cultivar ‘Kenya Heroe’. Seedlings of parents, F₁, F₂, F₃ and backcross populations from the two crosses were artificially infested with RWA in a greenhouse. The results indicated that the resistance in KRWAPC-8 was controlled by one dominant gene while two independent dominant genes governed resistance in KRWAPC-16 with recessive epistasis at both loci. The recessive epistatic gene action of KRWPC-16 has not been reported previously. Development of adapted cultivars incorporating different resistance genes may avoid development of RWA biotypes.

Media Summary

Two new sources of resistance to Russian wheat aphid from Turkey have been identified. Resistance in wheat KRWAPC-8 is conditioned by single dominant gene (Dnk) while two independently inherited dominant genes with epistatic effects (yet to be designated) govern resistance in wheat KRWAPC-16.

Key words

Russian wheat aphid, resistance, susceptible, segregation ratio, recessive epistasis.

Introduction

The Russian wheat aphid (RWA), Diuraphis noxia (Mordvilko) is one of the most damaging pests of small grains in the world. It was first reported in 1900 in the Mediterranean region and southern Russia and became a serious pest of wheat in South Africa in 1978. It rapidly spread to South America, USA and Canada and most parts of Europe. It has maintained minor pest status in Egypt, Sudan and Ethiopia but flared up in Kenya in 1995 where it remains the most important pest of wheat and barley. Severe infestation by RWA may result in yield losses up to 90% in commercial wheat cultivars (Kinyua et al., 2002). Feeding of RWA on susceptible cultivars causes leaf chlorosis, leaf rolling and purple coloration on the leaves. The effects on the plant are reduced plant height, sterile heads, low kernel weight, and in the most severe condition, death (Walters 1984). Control of the RWA with insecticide is neither environmentally safe nor economically effective although effective chemical control methods, using insecticides that combine contact with systemic or fumigant action to penetrate to the aphides in the rolled leaves, have been developed in South Africa. The use of resistant cultivars is a safe, effective and economical management option to protect wheat from RWA while minimizing the use of insecticides. Several thousand accessions of wheat and wheat relatives from the area where RWA is endemic have been evaluated for RWA resistance since 1987. There are at least 10 known genes for resistance to RWA, namely Dn1, Dn2, dn3, Dn4, Dn5, Dn6, Dn7 Dn8, Dn9, and Dnx (Elsidaing and Zwer 1993; Zhang et al., 1998; Nkongolo et al., 1991; Ehdaie and Baker 1999; Liu et al., 2001). Previous studies on allelic relationships among resistance genes remain inconclusive. Breeding of RWA resistant cultivars is further complicated due to presence of RWA biotypes. There are at least eight known biotypes worldwide (Puterka et al., 1992). In a recent study one of the winter wheat varieties, ‘Halt’, which is resistant in the USA and South Africa was highly susceptible while the other winter wheat line ‘PI 294994’ was found to be highly resistant in Kenya (Kiplagat et al., 2000). The objective of this study was therefore to evaluate and determine the genetic model of resistance to RWA in two Turkish wheat lines.

Materials and Methods

Plant Materials

The parental lines included two RWA resistant Turkish wheat lines, KRWAPC-8 and KRWAPC-16 (Kenya Russian Wheat Aphid Parental Collection) and the susceptible commercial cultivar, ‘Kenya Heroe’. Both resistant lines are agronomically very poor with low yields. The susceptible parent ‘Kenya Heroe’(P₁) was crossed with each of the two resistant parents, KRWAPC-8 and KRWAPC-16 (P₂). Seeds of F₁, F₂, F₃, and BC₁ P₁ (F₁ x P₁) were produced for each cross.

Greenhouse Screening

Seeds of P₁, P₂, F₁, F₂, F₃, and BC₁P₁ populations of each cross were planted in 1m long rows 0.2m apart in beds. Each row contained 15 plants. Number of rows in each population varied depending on the availability of seed. Seedlings were infested with three RWA per plant at the two-leaf stage using a paintbrush by placing the aphids in the whorl. The RWA damage (leaf chlorosis and leaf rolling) was scored on single plant basis 21 days after infestation on a 1-to-6 scale, 1 denoting healthy plants with isolated chlorotic spots, flat leaf and 6 denoting highly chlorotic, rolled and dying or dead plants. Plants with scores 1 to 3 were considered resistant and plant reactions 4 to 6 were considered susceptible.

Data Analysis

Chi-square values for 'goodness of fit ' to phenotypic segregation ratios of 3:1 (monogenic), 9:7 (digenic) in F_2,and 1:1 in BC₁P₁ (resistant: susceptible) were used to determine the genetic model of the RWA resistance genes in each of the two crosses. The randomly selected F₂:F₃ families were tested for ‘goodness of fit’ to the expected ratios of 1:2:1 (non-segregating resistant/segregating/non-segregating susceptible) for monogenic inheritance and 1:8:7 (non-segregating resistant /segregating /non-segregating susceptible) for inheritance governed by two dominant genes (digenic) with recessive epistasis. Other phenotypic segregation ratios were not appropriate to explain the observed segregations either in F₂, BC₁P₁ or F₃.

Results

The cross between ‘Kenya Heroe’ and KRWAPC-8

All seedlings of KRWAPC-8 were highly resistant (mean score of 2.2) and those of ‘Kenya Heroe’ were highly susceptible (mean score of 4.8). The F₁ seedlings were all resistant (mean score of 2.9) suggesting complete dominance of resistance over susceptibility. The F₂ population segregated in a 3 resistant: 1 susceptible ratio and the BC₁P₁ progeny segregated in a 1resistant: 1susceptible ratio, suggesting that RWA resistance is conditioned by single dominant gene. The F₃ family segregation in the ratio of 1resistant: 2segregating: 1susceptible further confirmed the model of a single dominant gene. Subject to confirmation through allelic tests the new resistance gene in KRWAPC is tentatively assigned a gene symbol ‘Dnk’.

The cross between ‘Kenya Heroe’ and KRWAPC-16

The F₁ seedlings from the cross between the susceptible parent ‘Kenya Heroe’ (mean score of 4.8) and the resistant parent KRWAPC-16 (mean score of 2.6) were all resistant with the mean score of 2.8. The F₂ population segregated in a 9:7 (resistant: susceptible) ratio indicating that two dominant genes condition the resistance in KRWAPC-16 with recessive epistatic effect to each other. The BC₁P₁ progenies segregated 1:1 (resistant: susceptible) providing further evidence that two independent dominant genes with epistatic effects govern resistance in KRWAPC-16. The F₃ family’s ratio of 1:8:7 (1 resistant: 8 segregating: 7 susceptible) support the F2 segregation data. The gene symbols for the two dominant RWA resistance genes in KRWAPC-16 will be assigned when they are confirmed by allelic tests with known resistance genes and monosomic studies.

Conclusion

Two new wheat lines of Turkish origin, KRWAPC-8 and KWAPC-16 were evaluated for inheritance of resistance to Russian wheat aphid at Njoro, Kenya. The genetic models of resistance in two lines were different. The resistance in KRWAPC-8 was controlled by a single dominant gene (Dnk) while the resistance in KRWAPC-16 was governed by two dominant genes with recessive epistasis.

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