Huerta-Espino J

Rebetzke GJ

Rosewarne GM

Singh RP

English

Sydney eScholarship

 1QTL identification in a slow-rusting population reveals complex inheritance patterns of resistance  Rosewarne GM1, Singh RP2, Huerta-Espino J3, Rebetzke GJ 1 1Plant Industry, CSIRO, Black Mountain, Canberra, Australia, 2International Maize and Wheat Improvement Center (CIMMYT), Apartado Postal 6-641, 06600, Mexico, D.F., 3Campo Experimental Valle de Mexico-INIFAP, Apdo. Postal 10, 56230, Chapingo, Edo. de Mexico, Mexico.  INTRODUCTION Slow-rusting or adult plant resistance genes that are effective against leaf and stripe rust can have significant impacts on disease severity in the field. Being quantitative and additive in nature, the combination of three or more of these genes into elite germplasm can provide very high levels of protection under epidemic conditions (Singh et al. 2000). To more effectively combine and deploy these resistance genes, it is important to know their chromosomal location. Many quantitative trait loci (QTL) have been identified as being important in reducing disease severity. There has been at least 18 loci identified as being effective against leaf rust and at least 15 effective against stripe rust (Rosewarne et al. 2008 and references therein).  Despite the identification of many slow-rusting loci, the majority have very minor effects against the diseases. However the loci, Lr34/Yr18 on chromosome 7D and Lr46/Yr29 on 1B, have reasonably significant effects against both leaf and stripe rust. Furthermore, the development of molecular markers to these genes has facilitated their identification in a range of germplasm. Although significant in their effect in reducing disease severity, alone these genes do not provide enough protection. Even when combined together, the resistance is usually not enough to combat the diseases to a sufficient level, unless combined with other background loci.  This study aims to identify slow-rusting loci in a F2 derived F5 SSD population from a cross between the susceptible Avocet and the slow-rusting line Attila. Field testing was completed over three seasons each for leaf rust and stripe rust (separately) under severe epidemic conditions. Partial linkage mapping was completed through a bulked segregant analysis. A multi-environment QTL analysis was conducted with QTLNetwork 2.0 (Yang et al. 2005). RESULTS Genetic analysis of this population indicated that at least two loci were involved in leaf rust resistance and at least three were involved in stripe rust resistance (Rosewarne et al. 2006). Furthermore, a significant QTL for both leaf rust reaction and stripe rust reaction was observed across all environments and located to chromosome 1BL (Fig 1). This was shown to be Lr46/Yr29 through its co-location with leaf tip necrosis and several molecular markers diagnostic for this locus. This QTL had the highest additive effect for rust reaction against both leaf rust (27.2) and stripe rust (13.2) Table 1 and 2.  There were two other loci that had minor but significant effects on leaf rust reaction (Fig. 1, Table 1). These were located on chromosome 2BS and 7BL. These loci, along with the Lr46/Yr29 locus, accounted for nearly 70% of the phenotypic variation observed for leaf rust.  There were six QTL associated with stripe rust reaction (Table 2), one of which showed a significant genotype × environment interaction. Loci were identified on chromosome 1BL (Lr46/Yr29), 2BS, 2BL, 7BL and two unidentified regions. The 1BL, 2BL, 7BL and an unmapped locus had consistent effects across all environments. The 2BS locus had a significantly larger effect on reducing disease severity in the second year of stripe rust data. Another unmapped locus had an epistatic effect by reducing stripe rust reaction associated with the Lr46/Yr29 locus. DISCUSSION Slow-rusting resistance to leaf rust in this population was relatively straight forward with three loci contributing to resistance. The Lr46/Yr29 locus was the dominant contributor and accounted for an average reduction in disease severity of over 54%. Two other loci had minor but consistent effects of leaf rust reaction. This is interesting as genetic inheritance analysis predict a minimum of two genes being involved in resistance. A flaw of this type of analysis is that it assumes all loci contribute equally to resistance but this is clearly not the case. It cannot be ruled out that other minor genes may also be involved in resistance.  Previous studies have shown QTL for leaf rust reaction on 2B and 7B (see numerous references in Rosewarne et al 2008). This indicates that these regions are important sites for slow-rusting resistance to leaf rust and may be widespread in a range of germplasm.  Stripe rust resistance was much more complicated in this population. Again the Lr46/Yr29 locus had a significant contribution, giving an average reduction in disease  2 severity of over 26%. However, four other loci also contributed to resistance. Of the other loci, the 2BL is of interest as no previous studies had identified this region as being important for stripe rust. This locus and one other that could not be chromosomally localised were derived from the susceptible parent, Avocet. Singh et al. (2005) had identified resistance on 6A from Avocet. A possible reason why neither locus was identified by both Singh et al (2005) and in this study, could be due to the use of partial linkage mapping. This commonly results in incomplete genome coverage, so that QTL with minor effects may be overlooked.  The other locus derived from the Avocet parent was not able to be mapped as it was only identified through AFLP based markers. Therefore, although it was not linked to the 2BL linkage group, conclusions as to whether it was associated with the 6A locus of Singh et al (2005) cannot be drawn.  The QTL on 2BS was most intriguing as it showed a significant environmental interaction. In 2002, it accounted for an additive effect of 9.3%. However, this effect was much lower in the other 2 years (4.7% and 5.5%). Field notes taken in 2002 revealed an early incursion of an endemic Yr27 avirulent stripe rust pathotype, followed up by the spread of the inoculated Yr27 virulent pathotype. As Attila is known to contain Yr27, it seems likely that this gene was involved in the QTL observed in 2002. Interestingly, the smaller additive effects in 2000 and 2003 may be indicative of low levels of this endemic rust pathotype being present.   The 7BL QTL for stripe rust reaction was consistently observed in all three years. Suenaga et al. (2003) also identified a QTL in this region and this may be a useful locus in helping to generate high levels of resistance based on slow-rusting.  Finally one other locus that came from an AFLP based linkage group had an epistatic interaction with stripe rust reaction from Lr46/Yr29. When both loci were present this locus accounted for a decrease in additive effect of 7%. This was significant and present in all three environments. The presence of such genes in slow-rusting lines indicates the value of breeding and selecting material under epidemic conditions, as was the case with the development of Attila.  In conclusion, the inheritance of slow-rusting was relatively simple for leaf rust reaction with only a few genes being involved. Resistance to both rusts was generally dominated by the effect of the Lr46/Yr29 locus. However, stripe rust resistance was much more complicated with a total of 7 loci being involved. Some of these loci were derived from the susceptible parent and one was epistatic in function. With the advent of molecular markers for the two dominant slow-rusting genes of Lr34/Yr18 and Lr46/Yr29, the incorporation of these two loci in breeding material will be easier to achieve. However these are unlikely to provide adequate protection for stripe rust unless other minor genes are incorporated. REFERENCES Rosewarne GM, Singh RP, Huerta-Espino J, William HM, Bouchet S, Cloutier S, McFadden H, Lagudah ES (2006) Leaf tip necrosis, molecular markers and 1-proteasome subunits associated with the slow rusting resistance genes Lr46/Yr29. Theor Appl Genet 112:500-508 Rosewarne GM, Singh RP, Huerta-Espino J, Rebetzke RJ (2008) Quantitative trait loci for slow-rusting in wheat to leaf rust and stripe rust identified with multi-environment analysis. Theor Appl Genet 116: 1027-1034 Singh RP, Huerta-Espino J, William HM (2005) Genetics and breeding for durable resistance to leaf and stripe rusts in wheat. Turk J Agr Forest 29:121-127 Singh RP, Huerta-Espino J, Rajaram S (2000) Achieving near-immunity to leaf and stripe rusts in wheat by combining slow rusting resistance genes. Acta Phytopathol et Entomol Hungarica 35:133-139  Suenaga K, Singh RP, Huerta-Espino J, William HM (2003) Microsatellite Markers for genes Lr34/Yr18 and other quantitative trait loci for leaf rust and stripe rust resistance in bread wheat. Phytopathology 93:881-890 Yang J, Hu CC, Ye XZ, Zhu J (2005) QTLNetwork 2.0. Institute of Bioinformatics, Zhejiang University, Hangzhou, China (http://ibi.zju.edu.cn/software/qtlnetwork)                3Table 1 Multi-environment QTL analysis for leaf rust (LR) reaction in the Avocet-S × Attila population. Estimated additive effects are given for significant leaf rust reaction QTL in all environments and deviations from this value for individual environments. Negative values indicate the resistance allele is derived from the susceptible parent  QTL Chromosome Lr Lr Lr Lr  interval/marker location All 2000 2002 2004  XP84/M78-LTN 1BL 27.2 -0.5 1.5 -1.1  Xgwm682-XP32/M62 2BS 4.4 0.0 0.0 0.0  Xwmc273-Xgwm146 7BL 3.0 -0.4 1.4 -1.0 Table 2 Multi-environment QTL analysis for stripe rust (YR) reaction in the Avocet-S × Attila RIL population. Estimated additive effects are given for significant stripe rust reaction QTL in all environments and deviations from this value for individual environments. Negative values indicate the resistance allele is derived from the susceptible parent. * significantly different from mean additive effect at P<0.1 and ** at P<0.01; nd = not determined   QTL Location Yr Yr Yr Yr  Interval/Marker  All 2000 2002 2003  LTN-XP35/M55 1BL 13.2 -0.7 -1.1 1.8  XP32/M62-XP88/M64 2BS 6.5 -1.8 2.8* -1.0  Xgwm1027-Xgwm619 2BL -4.5 -0.6 1.5 -1.0  XP32/M59-Xgwm344 7BL 3.1 0.0 0.0 0.0 XP87/M68b-XP85/M67b nd -3.1 0.0 0.0 0.0  XP33/M61 nd 4.8 2.3* -3.3** 1.0   Figure 1 Loci identified as having effects against leaf rust reaction (Lr) stripe rust reaction (Yr).  XP33/M55XP35/M55XP84/M78XP85/M67XP33/M598 8 YrLTN11 35 8 Lr2 612 31BL Xwmc10Xgwm344XP32/M59Xgwm146Xwmc273Xgwm5777 212 0 Yr11 820 5 Lr7 67BLXwmc257Xwmc154Xgwm682XP88/M64XP34/M59XP32/M62Xgwm120Xgwm501XP84/M6820 820 122 3 Lr19 5 Yr23 725 414 18 92BS Xgwm1027Xgwm6191 7 Yr2BL  4  

QTL identification in a slow-rusting population reveals complex inheritance patterns  of resistance

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QTL identification in a slow-rusting population reveals complex inheritance patterns of resistance

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