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Crop Science 40:1148-1155 (2000)
© 2000 Crop Science Society of America

CELL BIOLOGY & MOLECULAR GENETICS

Mapping Yr28 and Other Genes for Resistance to Stripe Rust in Wheat

R.P. Singha, J.C. Nelsonb and M.E. Sorrellsc

a Wheat Program, International Maize and Wheat Improvement Center (CIMMYT), Apdo. Postal 6-641, 06600 Mexico, D. F., Mexico
b 49 Lionel Rd., Darlington WA 6070, Australia
c Dep. of Plant Breeding and Biometry, 252 Emerson Hall, Cornell Univ., Ithaca, NY 14853, USA

jcnelson{at}global.net.au


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 Materials and methods
 Results
 Discussion
 Conclusion
 REFERENCES
 
Stripe (yellow) rust, caused by Puccinia striiformis West., is an important constraint to wheat production in cool environments. With the purpose of identifying genes for resistance to the disease, a RFLP mapping population of recombinant inbred lines developed from a synthetic [Triticum turgidum L. x Aegilops tauschii (Coss.) Schmal.] x T. aestivum L. cv. `Opata 85' cross was visually evaluated for seedling infection type in three greenhouse inoculation tests and for adult-plant disease severity in four field tests at Celaya and Toluca, Mexico. A previously unidentified gene from Ae. tauschii, designated as Yr28, was located on chromosome arm 4DS. Although Yr28 strongly influenced seedling resistance, it showed a strong effect in adult plants at only the warmer of the two field sites. A second gene showed high environmental sensitivity in seedling tests, with resistance associated with Opata marker alleles near the adult-plant resistance (APR) gene Yr18 on chromosome arm 7DS. Gene Yr18, known to be present in Opata, strongly reduced disease response in field trials and was tightly linked with leaf-rust resistance gene Lr34. Three other regions from Opata on chromosome arms 3BS, 3DS, and 5DS were also associated with APR.

Abbreviations: APR, adult-plant resistance • At, Aegilops taushii • IT, infection type • RFLP, restriction fragment length polymorphism • RIL, recombinant inbred line • YR, yellow or stripe rust


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
Materials and methods
 Results
 Discussion
 Conclusion
 REFERENCES
 
OF THE THREE RUST DISEASES of wheat, stripe (yellow) rust (YR) is the most damaging to grain yields in cool, moist environments. Chemical control of rusts is expensive and hazardous to the environment. The primary focus of breeding for disease control is now durable (Johnson, 1988) genetic resistance, which often involves race-nonspecific, slow-rusting (Caldwell, 1968) mechanisms and is best identified in the adult-plant stage. Race-specific resistance, expressed as a low infection type in seedling tests, often proves short lived in the field (Kilpatrick, 1975) owing to genetic shifts or the emergence of new virulences in the pathogen population in response to host selectivity.

Race-nonspecific YR resistance is reported in the literature, with cultivars carrying such resistance listed in Roelfs et al. (1992). One gene identified as a key contributor to the slow rusting of several wheat cultivars of CIMMYT origin is Yr18 (Singh and Rajaram, 1994). This gene is tightly linked to the slow-rusting and durable leaf rust (P. recondita Roberge ex Desmaz. f. sp. tritici (Eriks & E. Henn.) D.M. Henderson) resistance gene Lr34 (McIntosh, 1992; Singh, 1992a). In common with typical APR genes, both Yr18 and Lr34 display a moderately high or compatible infection type on seedlings and a disease-lowering or -delaying effect with increasing plant maturity (Dyck and Samborski, 1982; Singh, 1992a). In field conditions, both genes exert only partial control which is unsatisfactory under high disease pressure. Consequently, both are best combined with other slow-rusting genes (Ma and Singh, 1996; Singh and Huerta-Espino, 1997).

Identification and characterization of minor slow-rusting resistance genes is difficult by classical methods. Recently, RFLP maps of wheat chromosomes were constructed (Van Deynze et al., 1995; Nelson et al., 1995a, b, c; Marino et al., 1996) in a population of recombinant inbred lines (RILs) developed from a synthetic hexaploid x bread-wheat cross. This genetic material has been used to characterize and map resistance genes for other diseases (Nelson et al., 1995b, 1997, 1998; Faris et al., 1997). The synthetic parent was reported to carry YR resistance (Ma et al., 1995) and should be a source of valuable genetic diversity for bread wheat cultivar improvement.

The objective of this study was to identify wheat chromosomal regions carrying stripe rust resistance genes effective at seedling and adult-plant stages by using the available mapping population and RFLP map.


   Materials and methods
TOP
 ABSTRACT
 INTRODUCTION
 Materials and methods
Results
 Discussion
 Conclusion
 REFERENCES
 
Germplasm
The study was conducted on 131 F7 RILs developed by single-seed descent from the F2 generation of a cross between a synthetic hexaploid wheat and the Mexican spring bread wheat cultivar Opata 85 (Opata). The synthetic was reported (Nelson et al., 1995b) as having been produced from a cross between the durum wheat cultivar Altar 84 (Altar) and the Ae. tauschii (hereafter At) CIMMYT accession W-219. However, some recent results (R.P. Singh, 1998, unpublished data; and see below) indicate that this pedigree may not be correct.

Testing for Seedling Resistance
The lines, parents, and stripe rust differentials were planted as clumps of 6 to 8 seeds in trays. Ten-day-old seedlings were inoculated by spraying with a 2 to 3 mg/mL suspension of urediniospores suspended in light mineral oil (Soltrol 170, Phillips 66 Co., Bartlesville, OK). The inoculated trays were placed in water in closed transparent boxes in a chamber maintained at 12°C. Seedlings were misted through an inlet until sufficient dew was formed and incubated for 12 h under dark. Incubation was continued for an additional 24 h under light at the same temperature, and the trays were then transferred to benches in a greenhouse maintained at 15 to 18°C. Natural daylight was supplemented with additional light to provide 14-h days.

The first pathotype of P. striiformis used in inoculations was 14E14 (Johnson et al., 1972), which is virulent to resistance genes Yr2, 3, 6, 7, 27, and A and was the predominant pathotype in the Mexican highlands until 1996. The second pathotype, CIMMYT accession MEX96-11, is not fully classified on the differential set of Johnson et al. (1972) but has the following avirulence/virulence formula (based on the spring wheat near-isogenic lines in cv. Avocet recently developed by C.R. Wellings and R.A. McIntosh, Plant Breeding Institute, The University of Sydney, Australia): Yr1, 4, 5, 8, 15, 17/ 2, 3, 6, 7, 9, 10, 27, A. Infection type (IT) was recorded on a 0- to-9 scale (McNeal et al., 1971) about 18 d after inoculation. On this scale, 0 represents no visible symptom; 1, necrotic or chlorotic flecks without sporulation; 2, necrotic or chlorotic blotches without sporulation; 3, necrotic or chlorotic blotches with trace sporulation; 4, necrotic or chlorotic blotches with light sporulation; 5, necrotic or chlorotic blotches or stripes with moderate sporulation; 6, chlorotic stripes with moderate to abundant sporulation; 7, stripes without chlorosis and with moderate sporulation; 8, stripes without chlorosis and with abundant sporulation; 9, stripes with profuse sporulation.

Independent seedling tests were carried out with both pathotypes from December 1995 to January 1996 and repeated with pathotype MEX96.11 from September to October 1997. In the 1996 tests, air-conditioning failure caused an increase in temperatures up to 25°C for an unknown length of time during the day over a 4-d period.

Disease Testing in Adult Plants
Field YR testing was carried out in Mexico at Celaya (Guanajuato state) during the winter season of 1993 to 1994, and at Toluca (Mexico state) during the summer seasons of 1994 and 1997. Lines were planted in plots at 3 g seed per plot yielding about 60 plants in two 1-m rows seeded 15 cm apart, with 70 cm between plots. The susceptible spreader cultivar Morocco was planted as hills in the middle of a 1-m pathway on one side of each plot. For epidemic initiation, spreader rows were sprayed with urediniospores suspended in oil. Pathotype 14E14 was used in Celaya and during the 1994 season in Toluca, whereas pathotype MEX96-11 was used during the 1997 season at Toluca. Disease severity was recorded at each location when the flag leaves of the susceptible check, Avocet, displayed approximately 100% severity based on the modified Cobb scale (Peterson et al., 1948). Data were recorded only once in 1994 trials but twice in the 1997 trial, the second time after leaves of Avocet were necrotic from the disease. Infection type on flag leaves, based on the 0-to-9 scale (McNeal et al., 1971), was recorded only at Celaya where rain during the crop season is rare. Recording correct infection type at Toluca is difficult due to the washing effect of high rainfall during the crop season.

Data Analysis
About 450 RFLP markers from the mapping studies cited above were used and were distributed over the 21 wheat chromosome maps at an average spacing of 8 cM; however, most of the maps have at least one 20- to 30-cM gap. Marker data were available for 114 of the lines. Both IT and severity data were analyzed with simple and interval (Haley and Knott, 1992) regression mapping, except for IT partitioned into susceptible and resistant classes, for which chi-square tests were made as described in Nelson et al. (1997). A nominal genome-wide significance level of LOD 3.2 corresponding to P = 0.05 (Lander and Botstein 1989) was confirmed by permutation tests (Churchill and Doerge, 1994). Disease scores were reshuffled 10 000 times with respect to marker genotypes, each shuffle being followed by recomputation of the chromosome interval maps and recording of the maximum LOD across all chromosomes. Calculations were done by QGene (Nelson, 1997).

Strictly IT data are only semiquantitative, ordinal data; however, regression interval mapping with such data is satisfactorily robust under all but extreme conditions (Rebaï, 1997) and here gave results qualitatively similar to those of nonparametric tests.


   Results
TOP
 ABSTRACT
 INTRODUCTION
 Materials and methods
 Results
Discussion
 Conclusion
 REFERENCES
 
Seedling Resistance
The infection types displayed by the parents tested with P. striiformis pathotypes 14E14 and MEX96.11 are presented in Table 1 . The synthetic and its nominal durum parent Altar gave resistant seedling responses (IT ranging from 2–3 to 3–4) to both pathotypes in each test, while Opata gave a moderately susceptible response (IT 6–7 to 7–8). The At parent of the synthetic was not included in tests owing to lack of seed.


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  		Table 1 Infection type displayed by parents of Synthetic x Opata wheat RILs when 10-d-old seedlings were inoculated with two pathotypes of P. striiformis in independent tests

 
Segregation Analysis of IT Scores
In the seedling tests for both pathotypes tested in 1996, when progeny displaying ITs ranging from 1 to 2 to 4 to 5 were scored as resistant and those with higher ITs as susceptible, the classes were distributed in a 3:1 ratio (Fig. 1) indicating that two independent genes conferred resistance. Because the resistant and susceptible responses of progeny lines were similar with both pathotypes (data not shown), it was concluded that the same genes (called here for convenience X and Y) were involved. All lines susceptible in 1996 seedling tests were again susceptible in the 1997 test with pathotype MEX96.11, but now responses were distributed in a 1:1 ratio (Fig. 1) indicating that only gene X was conferring seedling resistance and Y not expressing. Genotypes assigned based on IT scores for the two tests showed a distribution of 63 XX– – : 27 xxYY: 32 xxyy, consistent with a 2:1:1 genetic ratio ( , P < 0.75).



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  		Fig. 1 Infection type (IT) distribution of Synthetic/Opata wheat recombinant inbred lines tested with two pathotypes of P. striiformis. The bars labeled "Cumul[ative]" R and S are inserted to illustrate the 3:1 and 1:1 segregation ratios for the pooled resistant vs. susceptible line classes

 
Assignment of Yr28
Marker analysis of IT by either regression on unpartitioned IT scores or contingency test of partitioned IT data indicated X, the gene from the At parent expressed in all seedling tests, to be an allele of a major resistance gene distal on chromosome arm 4DS. We have named this gene Yr28. In the 1996 test with pathotype 14E14, RFLP Xmwg634-4D (Table 2 , Fig. 2) accounted for about 32% of IT variation with a mean reduction of almost IT 3 levels favoring the At homozygote. Of 55 lines with the At allele at Xmwg634-4D only 3 gave susceptible IT, whereas in lines with the Opata allele resistance segregated in a 1:1 ratio as expected due to segregation of the second gene Y.


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  		Table 2 Contingency tests for chromosome arm 4DS and 7DS marker associations with seedling stripe rust infection type scored as a binary trait in Synthetic/Opata wheat RILs

 


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  		Fig. 2 Chi-square contingency-test contours for seedling stripe rust IT scored as a binary (R, S) trait in Synthetic/Opata wheat RILs. Key to plot labels: 1 4E14_RS, response to race 14E14 at standard temperatures; Yr28, Yr18', resistance responses of these assigned genes to challenge with race MEX96-11. Markers are arrayed in map order with short arms of chromosomes at right. Chromosome lengths reflect numbers of markers, not genetic length

 
Regression analysis of the 50 lines scored for seedling IT, after removal of the 56 resistant lines carrying the At marker allele at Xmwg634-4DS, showed a reduction of 2 IT levels associated with the Opata allele of a 7DS locus near Xbcd1438 (Fig. 3) . Since this region has previously (Nelson et al., 1995c, 1997) been associated with APR to leaf rust conferred by gene Lr34, the effect suggested the action of Yr18, which is present in Opata and known (Singh, 1992b) to be tightly linked to Lr34. Several minor marker associations also suggested in Fig. 3 are not described here. In what follows, the seedling gene referred to above as Y is designated Yr18', owing to uncertainty (see below) as to its identity with Yr18.



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  		Fig. 3 Contours showing LOD for simple regression of seedling IT in Synthetic/Opata wheat RILs on each RFLP marker in turn, after removal of resistant lines carrying the Synthetic allele at RFLP marker Xmwg634-4DS, and chi-square contingency test for the same trait coded as binary (R, S). Markers are arrayed in map order with short arms of chromosomes at right. Chromosome lengths reflect numbers of markers, not genetic length. In the upper (LOD) plot, deviation from center line at a marker indicates the parent contributing the allele associated with higher disease

 
In the September 1997 test with pathotype MEX96.11 giving the 1:1 resistant/susceptible distribution indicating single-gene segregation, the same 4DS region was again prominent. We speculate that the expression of Yr18' in only the earlier tests was owing to the higher temperatures resulting from the air-conditioning failure mentioned above. Though expression only at higher temperatures is not uncommon with rust-resistance genes, a definitive conclusion about the expression of this gene requires testing under strict temperature control.

Adult-Plant Resistance (APR)
Stripe rust severity of the synthetic was rated as 0 and 1, of Opata as 30 and 40, and of Altar durum as 0 and 0 on the two dates data were recorded in 1997 trials at Toluca. Parents were not included in the 1994 Toluca trial, and only the synthetic (10% severity) and Altar (35%) in the Celaya trial. In all trials, the responses were distributed in a continuous manner with low to high severities (Fig. 4) indicating that the segregation of resistance was complex. At least in the 1997 Toluca trial where a susceptible check cultivar Avocet S was included in the beginning and the end of the trial, none of the lines could be considered as susceptible as the check. Avocet had dead leaves from stripe rust at a second scoring on 8 August; however, the three most susceptible lines displayed only 80% severity (Fig. 4). The deficit of susceptible lines is consistent with the segregation in this cross of at least six independent resistance genes (124 R : 0 S lines, , P > 0.1), or alternatively the presence of one or more minor genes common to the synthetic and Opata parents. The continuous distribution and 25 lines displaying severity of 0 to 1 support the action of an array of resistance genes.



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  		Fig. 4 Distribution of Synthetic x Opata wheat RILs for field stripe rust severity at two locations. Severity scores are based on the modified Cobb scale (Peterson et al., 1948)

 
The range and mean severity in lines with or without genes Yr28 and Yr18' (as assigned from seedling IT) are given in Table 3 . The presence of Yr28 reduced disease severity by up to one third in both of the Toluca trials but had only a slight effect in the Celaya trial. In contrast, presence of the Yr18–7DS region from Opata reduced severity by almost half in all trials. Noteworthy here is that 32 lines judged from seedling IT to lack both of the above genes were not susceptible in the adult stage but had continuously distributed responses across a low to high severity range. This indicates the presence of two or three additional genes with cumulative effects together with Yr28 and Yr18'.


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  		Table 3 Range and mean stripe rust severities of Synthetic x Opata wheat RILs in the presence and absence of genes Yr28 and Yr18' when tested at two field locations

 
The APR to YR at the field location in Celaya was associated with regions on chromosomes 3BS and 7DS and that at Toluca with regions on 3DS, 4DS and 7DS (Fig. 5 and 6) . All pronounced resistance effects were contributed by Opata with the exception of the 4DS one, from Yr28 (Table 4) . Both the 4DS At and 7DS Opata RFLP alleles were those implicated in seedling resistance. The observed effect of Yr18 was greater in Celaya than in Toluca in 1994 trials (Table 4). The Yr28-4DS region involved in seedling resistance was detected in the adult-plant stage only at Toluca, where it reduced rust severity by up to 30%, expressed as difference between means of opposite homozygotes. The distal 3BS region influencing stripe rust in the field at Celaya was the same associated with resistance to leaf rust from Opata gene Lr27 (Nelson et al., 1997). Both Yr28 and the 3BS gene lowered both IT and disease severity.



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  		Fig. 5 LOD contours for simple regression of field stripe rust severity in Synthetic/Opata wheat RILs on each RFLP marker in turn. Markers are arrayed in map order with short arms of chromosomes at right. Chromosome lengths reflect numbers of markers, not genetic length. Deviation from center line at a marker indicates the parent contributing the allele associated with higher disease

 


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  		Fig. 6 Interval regression LOD contours for adult-plant stripe-rust resistance associated with four chromosome arms in Synthetic/Opata wheat RILs

 

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  		Table 4 Estimated disease reduction associated with resistance allele at putative stripe-rust resistance loci in Synthetic/Opata wheat RILs

 
A minor but consistent reduction in field disease (up to 25% severity and R2 = 0.14) as well as in seedling IT was associated with Opata alleles on chromosome 5DS proximal to the kernel hardness gene ha carried by Opata on that arm (Fig. 5). Another such Opata-derived effect was that from 3DS (Fig. 5 and 6), but this was pronounced (R2 = 0.14) only in one of the Celaya trials and minor in others. Neither of these two genomic regions has been found to be associated with any other resistance gene in studies using this population.


   Discussion
TOP
 ABSTRACT
 INTRODUCTION
 Materials and methods
 Results
 Discussion
Conclusion
 REFERENCES
 
Inheritance of Resistance at Seedling Stage
A previously unidentified stripe-rust resistance gene from Ae. tauschii located on wheat chromosome arm 4DS was designated as Yr28. In segregating progeny, this gene conferred ITs ranging from 1–2 to 4–5, indicating that the genetic background affected the level of resistance expression.

Although Altar, the nominal durum component of the synthetic, was resistant in all seedling tests, the progeny showed no significant evidence of carrying a resistance gene derived from the durum A or B genomes. If the D genomes of At and of Opata carry the same suppressing allele, resistance of Altar could remain suppressed in a hexaploid. We earlier reported (Nelson et al., 1997) that At accession 219 carries a suppressor for leaf-rust resistance gene Lr23, present in Altar, while Opata carried a non-suppressing allele that allowed the expression of Lr23 in one fourth of the progeny lines. A second unknown leaf rust resistance gene present in Altar and effective against all Mexican P. recondita pathotypes remained apparently suppressed in the synthetic and the recombinant inbred lines.

We now suspect on the basis of the present results and unpublished observations of the first author that Altar 84 is not in fact the durum component of the synthetic. A repeated failure of known rust-resistance infection types from Altar to appear in the progeny of a synthetic hexaploid derived from this cultivar is less plausible than a mixup of parents at an early stage of construction of the synthetic or of the recombinant inbred population. We are unable to determine the origin of Ae. tauschii accession W-219. Until a reliable identification of the components of the synthetic parent has been made, for example by DNA fingerprinting of an assortment of CIMMYT durums and synthetics, we cannot trace to their source germplasm any genes shown to be carried by the synthetic parent. Though unfortunate, this circumstance does not prevent their use in breeding.

The apparently identical chromosome locations suggest that the seedling-resistance gene we refer to above as Y or Yr18' is identical to APR gene Yr18. If this were so, however, the Yr18-carrying bread-wheat parent Opata should show a low seedling IT instead of the moderately susceptible IT that it consistently displays. For this reason, we leave unresolved the relationship between these two resistances.

Possible Influences on APR
Replicating the disease tests at the studied locations might have permitted a comparison of within-site with between-year variation, for example with respect to the 3DS and 5DS effects that were observed in only some trials. However, we propose that qualitative variations in resistance-gene expression were due to macroenvironmental (across-year) and not to microenvironmental variation. This proposition is based on the uniformity of disease pressure with the spreader method used and on previous observation in this material (Nelson et al., 1997) including the detection of known rust resistances even under natural epidemics. Epidemics were almost certainly monotypic, as in neither Mexican field location do natural YR epidemics occur. At Celaya, no other diseases occur to confound disease evaluation, while scoring at Toluca was terminated before the late-season onset of septoria tritici [Mycosphaerella graminicola (Fuckel) J. Schröt. in Cohn (anamorph Septoria tritici Roberge)] blotch.

Similarly, repeated rust evaluations during the growing season might have given information on the temporal variation in expression of resistance genes. For example, of four pronounced leaf-rust resistance gene effects evident at around 85 d after planting at Ithaca, NY, in 1994 (Nelson et al., 1997), gene Lr23 was not detected in a marker analysis of disease readings taken 3 wk earlier (data not shown). In our study, the distances of field sites, mainly Celaya, from CIMMYT headquarters made repeated scoring impractical.

Does Yr28, the single gene of Synthetic origin found in the inbred lines, account for the high resistance of this parent to the pathotypes used? A hint at the assortment of minor genes that may contribute to this resistance may be seen in Fig. 3, where most of the lines carrying Yr28 have been removed from the analysis.

Coincidence of Resistance Genes for Different Foliar Diseases
Slow-rusting genes Yr18 and Lr34 are reported to be closely linked not only with a leaf-tip necrosis gene Ltn (Dyck, 1991; Singh, 1992a) but with a non-suppressor of stem-rust resistance (Dyck, 1987) and with Bdv1 (Singh, 1993), a gene conditioning slow yellowing response to barley yellow dwarf virus. If the same locus is responsible for all of these resistances, their race- and pathogen-nonspecificity suggests that the APRs associated with the locus involve not specific recognition of the pathogen, but some more general cellular inhibition of invasion.

Resembling the complex of Lr34/Yr18/Ltn in conditioning resistance to all three wheat rusts is that of Lr27, which is tightly linked to Sr2, a durable APR gene against stem rust (Singh and McIntosh, 1984). It appears from our results that this genomic region, which was associated with both field and seedling resistance to leaf rust (Nelson et al., 1997) also reduces YR IT and, to a lesser degree, disease severity in the field. Further evidence that the resistances conferred by both 7DS and 3BS loci are not only race- but pathogen-nonspecific is a marked association of Opata marker alleles for both loci with field resistance to powdery mildew (Erysiphe graminis DC f. sp. tritici Ém. Marchal) (J.C. Nelson, 1996, unpublished data).

Complex resistance loci carrying numerous highly homologous variants of a DNA sequence are of common occurrence in crop species. Gene amplification may arise from unequal recombination under natural selection exerted by disease pressure (Bennetzen and Hulbert, 1992). However, complexes such as the flax M locus (Mayo and Shepherd, 1980) and lettuce downy-mildew loci (Hulbert and Michelmore, 1985) seem to mediate exclusively race-specific recognition of a single pathogen. A step toward elucidating the resistance mechanism(s) associated with the wheat APR complexes described here will be the acquisition of their DNA sequences.

Temperature Sensitivity of Resistance Expression
The APR in the progeny was complex and quantitative, appearing to be influenced by several chromosomal regions. The most prominent region was that of gene Yr18 on chromosome 7DS from Opata, which could be detected at both locations and in each test. The At gene Yr28 on 4BS was effective in adult plants only at Toluca, which is a high-rainfall, summer-planted location with temperatures ranging mostly between 10 to 22°C and longer day length through most of the season. Celaya, a winter-planted location, has shorter day length and temperatures ranging between 5 and 20°C during the first half of the cycle followed by increasing temperatures and day lengths. This suggests that the expression of Yr28 in the adult-plant stage is sensitive to temperature or other environmental factors. Such environmental influence was not seen in the seedling tests. In contrast gene Yr18' was temperature sensitive in the seedling stage but Yr18, either identical or closely linked to Yr18', conferred useful resistance at both field sites. Stripe-rust APR genes are commonly more effective at higher temperatures (Qayoum and Line, 1985; Broers et al., 1996); the same may be true for Yr28. By comparison, although the leaf-rust resistance gene Lr34 confers moderate IT at low temperatures and low light intensity, its effectiveness in both seedlings and adult plants gradually decreases with increase in temperature (Singh, 1992b; Drijepondt and Pretorius, 1989).


   Conclusion
TOP
 ABSTRACT
 INTRODUCTION
 Materials and methods
 Results
 Discussion
 Conclusion
REFERENCES
 
We have identified and mapped a new gene from Aegilops tauschii, designated Yr28, that contributes to seedling and field resistance to the predominant race of stripe rust in the Mexican highlands and appears to increase in effectiveness at higher field temperatures. Long experience with seedling-expressed genes, however, suggests that Yr28 would be overcome by new pathogen races unless combined with other race-specific or durable genes such as Yr18. The genomic proximity of leaf rust APR gene Lr34 to stem- and stripe-rust resistance genes appears to be paralleled by that of Lr27 to Sr2 and an as-yet unnamed YR APR gene. Yet to be resolved are the role of the Yr18 putative gene complex in seedling resistance and that of minor resistance genes in enhancing resistance conferred on the Synthetic parent by Yr28. DNA-marker-based dissection of relationships between seedling and adult-plant resistance and environmental conditions offers the prospect of finer-scale management of the genetic competition between crop and parasite.


   ACKNOWLEDGMENTS
 
The 1994 planting and preliminary data analysis was done by J.E. Autrique. Assistance in collecting 1994 disease data in Celaya and Toluca trials was provided by L.H.M. Broers.

Received for publication April 29, 1999.


   REFERENCES
TOP
 ABSTRACT
 INTRODUCTION
 Materials and methods
 Results
 Discussion
 Conclusion
 REFERENCES
 




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