Crop Science Grow Your Career with CSSA
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Abstract Freely available
Right arrow Figures Only
Right arrow Full Text (PDF) Free
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via ISI Web of Science (9)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Ittu, M.
Right arrow Articles by Mustãtea, P.
Right arrow Search for Related Content
PubMed
Right arrow Articles by Ittu, M.
Right arrow Articles by Mustãtea, P.
Agricola
Right arrow Articles by Ittu, M.
Right arrow Articles by Mustãtea, P.
Crop Science 40:62-67 (2000)
© 2000 Crop Science Society of America

CROP BREEDING, GENETICS & CYTOLOGY

Association of Fusarium Head Blight Resistance with Gliadin Loci in a Winter Wheat Cross

Mariana Ittua, Nicolae N. Sãulescua, Ioana Hagimaa, Gheorghe Ittua and Pompiliu Mustãteaa

a Research Institute for Cereals and Industrial Crops (I.C.C.P.T.), Jud. Calarasi, 8264 Fundulea, Romania

saulescu{at}valhalla.racai.ro


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 Materials and methods
 Results and discussion
 REFERENCES
 
Fusarium head blight (FHB) is one of the major diseases of wheat (Triticum aestivum L.). Genetic control of resistance to Fusarium spp. has been studied in resistant Chinese spring wheat cultivars, but little is known about inheritance of lower but useful levels of resistance found in winter wheat. This study was undertaken to characterize the genetic control of FHB resistance and to identify possible associations of resistance with several marker loci in winter wheat. Recombinant inbred lines were derived from the cross of a susceptible winter wheat, F1054W, with a moderately resistant parent, Sincron, not related to the Chinese germplasm. The parents had different alleles at five marker loci, RhtB1, Rht8, W2, GliB1, and GliD1. Recombinant inbred lines were classified for alleles at the RhtB1 and Rht8 loci by plant height and seedling response to exogenous gibberellic acid. Alleles at the GliB1 and GliD1 loci were determined from the gliadin spectrum detected by starch gel electrophoresis and alleles at the W2 locus by phenotypes in the field. The area under disease progress curve (AUDPC) and relative weight of inoculated spikes (RWIS), following injection of Fusarium graminearum Schwabe inoculum into central florets of flowering spikes, were determined for 3 yr in the field. A significant increase in resistance was associated with the allele GliR1, suggesting location of a Fusarium head blight resistance quantitative trait locus (QTL) on chromosome T1BL.1RS. A smaller but significant increase in resistance was associated with allele GliD1b, indicating the presence of another QTL on chromosome 1D. No association between Fusarium resistance and RhtB1, Rht8, or W2 was found. The effects of favorable alleles on chromosomes 1B and 1D were cumulative. Selection for genotypes possessing GliR1 and GliD1b in this population would increase the probability of obtaining lines with higher resistance to Fusarium head blight.

Abbreviations: AFLP, amplified fragment length polymorphism • AUDPC, area under disease progress curve • FHB, Fusarium head blight • QTL, quantitative trait loci • RIL, recombinant inbred lines • RWIS, relative weight of inoculated spikes


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
Materials and methods
 Results and discussion
 REFERENCES
 
FUSARIUM HEAD BLIGHT wheat, caused by Fusarium spp., is a severe disease in warm and humid areas of the world (Parry et al., 1995; Gilchrist et al., 1997). In Romania, as in many temperate areas, the disease is sporadic but can be most damaging when moisture and humidity are present during anthesis (Ittu et al., 1997). Although complete resistance to FHB is unknown, large genotypic differences among cultivars are well documented (Liu, 1985; Liu and Wang, 1991; Mesterházy, 1997; Zhuping, 1994; Gilchrist et al., 1997; Ittu et al., 1998). However, the genetic basis of FHB resistance is still poorly understood, especially in winter wheat, and information on the chromosomal location of FHB resistance is scarce and contradictory (Buerstmayr et al., 1997).

Two genes were found to control FHB resistance in crosses with `Sumai 3' derivatives (Ban and Suenaga, 1997), and two or three resistance genes were identified in `Ning 7840' or `Frontana' (Singh et al., 1995; Van Ginkel et al., 1996), but quantitative inheritance was demonstrated in crosses with other cultivars (Snijders, 1990). Using monosomic analysis, Yu (1982) located genes for resistance to FHB in `Soo-mo3' on five chromosomes (2A, 5A, 1B, 6D and 7D), while Ban and Suenaga (1997), on the basis of the linkage with a suppressor gene for awnedness, located one of the resistance genes from Sumai 3 on the long arm of chromosome 5A or 6B. Buerstmayr et al. (1997) positioned FHB resistance genes in one Sumai 3 derivative on chromosomes 5A, 1B, 3B, 4B, 6B, and 6D and in another derivative on chromosomes 3A, 3B, 6B, and 4D.

Chromosomes 4A, 5A, 7A, 7B, 4D, 2A, 5B, 6B, 3D, and 7D were involved in controlling FHB resistance in cultivars Wangshiubai and Wenzhouhongheshang (Yu et al., 1986), and chromosomes 7A, 3B 5B, 6B, 6D, 3A, and 4D were found to control FHB resistance in five other Chinese cultivars (Yu, 1991). In a study of five sets of substitution lines, Grausgruber et al. (1997) found six chromosomes (4B, 3A, 6B, 5D, 2A, and 6D) with positive influence on the AUDPC and six chromosomes (5A, 6B, 2A, 7A, 4B, and 6D) with positive influence on the relative spike weight (infected spike weight/non-inoculated spike weight).

Bai et al. (1997) identified two QTL for scab resistance and several AFLP markers associated with these in recombinant inbred lines (RIL) derived by single-seed descent from a cross between the resistant Chinese wheat Ning 7840 and the susceptible cultivar Clark. Moreno-Sevilla et al. (1997) found 12 genomic regions containing putative QTL associated with FHB resistance in a population derived from a cross of Sumai 3 with `Stoa'.

While most research to date focused on Chinese germplasm, which possess the highest known levels of resistance, other sources of resistance can also provide effective protection against FHB and may complement deployment of Chinese-based resistance. This paper reports the inheritance of FHB resistance in a cross of two winter wheat parents having no detectable presence of the FHB-resistant Chinese germplasm in their parentage.


   Materials and methods
TOP
 ABSTRACT
 INTRODUCTION
 Materials and methods
Results and discussion
 REFERENCES
 
Response to artificial inoculation with Fusarium was studied in 108 RILs from a cross between winter wheat cultivars Sincron (moderately resistant to FHB) and F1054W(susceptible). Sincron was selected from the cross `Russalka'/`Aurora'/3/`Mexique50'/`B21'//Aurora/4/`Zg4163-73', as a long coleoptile, high-tillering semidwarf. The parentage of Sincron is not known to contain FHB-resistant Chinese germplasm (Fig. 1) . F1054W was selected from the cross `Montana'/3/Mexique50/B21//Aurora/4/`Lovrin32', as a semidwarf, high yielding line.



View larger version (18K):
[in this window]
[in a new window]
  		Fig. 1 Genealogy of Sincron winter wheat

 
From the F2 population, 108 spikes were randomly harvested and the seed was planted in the field as F3 head rows. From F3 to F7, one spike was harvested from each head row without any conscious selection and was used to plant the next generation. Seed from each F7:8 head-row was bulked to produce the recombinant inbred lines. Parents were homogeneous, so sampling from parents was not considered necessary.

Polymorphism was found among the parents, and consequently among the recombinant inbred lines, for height-reducing genes RhtB1 (previous designation Rht1) and Rht8, gliadin genes GliB1 and GliD1, and the gene W2, which controls the waxy appearance of leaves (Table 1) . Classification of parents and RILs according to alleles at RhtB1 and Rht8 was based on plant height and on seedling response to exogenous gibberellic acid, as measured by the height of two-leaf seedlings grown in sterilized sand and watered with Austin nutrient solution supplemented with 50 mg kg-1 gibberellic acid (Gale and Gregory, 1977). Alleles at the GliB1 and GliD1 loci were determined from the gliadin spectrum detected by starch-gel electrophoresis (Sozinov and Poperelya, 1980) in accordance to the allele designations published by McIntosh et al. (1993, 1998). Alleles at the W2 locus were determined by the phenotypes in the field. Only RILs which could be unambiguously classified according to the alleles at each marker locus were considered for the analysis of marker associations with FHB resistance. Consequently, the number of RILs included in the analysis for various markers was different (104 for RhtB1 and Rht8, 102 for GliB1 and GliD1, and 106 for W2). Segregation patterns for all marker loci fit the expected 1:1 ratio (0.25 < P < 0.90, data not shown).


View this table:
[in this window]
[in a new window]
  		Table 1 Marker loci showing polymorphism in the winter wheat cross Sincron/F1054W

 
Fusarium graminearum isolates were obtained by culturing naturally inoculated kernels collected from several regions of Romania. After purification, each isolate was assessed for aggressiveness in the seedling stage on three wheat cultivars previously known for their different response to FHB. Three of the most aggressive isolates (our collection numbers 8711, 8712, and 8713) were increased by continuous aeration for 7 d on liquid Czapek-Dox media (Mesterházy, 1977). Inoculum was obtained by mixing the same amount of each isolate, without any dilution, before inoculation. The inoculum represented a homogenized mixture of spores and mycelia, but no attempt was made to control the relative amount of spores, since isolates were selected directly for aggressiveness.

The 108 RIL were grown in the field on 5-m2 plots without replications, with parents repeated 10 times, during 1993, 1995, and 1996. While experimental variability inherent in field trials might have been reduced by growing RIL in more controlled conditions (e.g., in a greenhouse), data obtained in the field, from several years with different weather conditions, were considered more relevant for a breeding program.

Ten heads per plot were inoculated at anthesis, by injecting 0.5 mL of inoculum directly into each of four central florets of the spike with a veterinary mechanical syringe (Liu, 1985). Anthesis date varied among RIL by only 2 to 3 d, so that weather variation during inoculation time had little influence on results. Spread of infection within the inoculated heads (type II resistance as defined by Schroeder and Christensen, 1963) was assessed by AUDPC and RWIS. AUDPC was estimated by the formula suggested by Schaner and Finney (1977):

where yi is percentage infection at time ti.

With only two readings for the percentage of damaged spikelets in each inoculated head at 10 d (PDS10) and 20 d (PDS20) after inoculation, the formula becomes:

Mean AUDPC per plot was used for further analysis. RWIS was determined by weighing the ten inoculated spikes at maturity, and expressing this weight as a percentage of the weight of an equal number of non-inoculated spikes of similar size. Although AUDPC and RWIS are usually correlated, RWIS may reflect not only differences in resistance but also in tolerance to FHB.

Little spatial variation and no spatial trends were observed for AUDPC or RWIS among replicated plots of the two parents. Therefore, all plots were treated as a population in which markers were completely randomized, and comparisons were made among subsets of lines with alternative alleles at each locus. A t-test, assuming equal variances was used to determine the significance of differences between average values of recombinant lines grouped according to the alleles of the marker genes. A two-way ANOVA was used to test the significance of main effects and interactions for two-loci grouping of RILs. The significance of differences between means of individual lines and the mean of the most resistant parent was determined by a t-test based on genotype x years interaction in the error term.


   Results and discussion
TOP
 ABSTRACT
 INTRODUCTION
 Materials and methods
 Results and discussion
REFERENCES
 
Correlations for AUDPC readings among the three years were low (r = 0.36 to 0.48), suggesting a strong genotype x year interaction for Fusarium symptom expression (Table 2) . Correlations for RWIS readings were of similar magnitude (r = 0.39 to 0.46). The correlation between AUDPC and RWIS was highest between the average values across years (r = -0.74), lower for values within years (r = -0.52 to -0.75), and lowest among years (r = -0.30 to -0.47). All correlations were significant at the 0.01 probability level.


View this table:
[in this window]
[in a new window]
  		Table 2 Correlations among measures of Fusarium head blight resistance after artificial inoculation with Fusarium graminearum for 108 recombinant inbred lines from the winter wheat cross Sincron/F1054W

 
Frequency distributions for AUDPC of the 108 RILs indicated different patterns among years (Fig. 2) . In 1996, the bimodal distribution suggested segregation for one major gene. The distribution was skewed right, towards susceptibility, in 1993 (g1 = 0.61, P < 0.01), but did not significantly deviate from a normal distribution in 1995. The distributions for the two parents showed little overlap in 1993 and 1995, and no overlap in 1996 or for the 3-yr average. Frequency distributions for RWIS suggested quantitative inheritance, with significant skewness (g1 = 0.65, 1.03, and 0.71, in 1993, 1995, and 1996 respectively, P < 0.01) towards higher values in all years (Fig. 3) . No overlapping of parental distributions was observed in any year.



View larger version (30K):
[in this window]
[in a new window]
  		Fig. 2 Frequency distributions for the area-under-disease-progress curve (AUDPC) after artificial inoculation with Fusarium graminearum for 108 recombinant inbred winter wheat lines and two parents

 


View larger version (30K):
[in this window]
[in a new window]
  		Fig. 3 Frequency distributions for relative weight of inoculated spikes (RWIS) after artificial inoculation with Fusarium graminearum for 108 recombinant inbred winter wheat lines and two parents

 
Differences between parent means for both AUDPC and RWIS were signifficant (P < 0.01) in each year (Table 3) . With a mean AUDPC of 336 and mean RWIS of 59.3%, Sincron was less resistant than the Chinese spring wheat Sumai 3, which had a mean AUDPC of 208 and a mean RWIS of 78.7%, when tested in a nearby experiment by the same inoculation procedure. However, it has been our experience that such lower levels of resistance can provide significant field protection against FHB in most years, and can be used successfully in a breeding program.


View this table:
[in this window]
[in a new window]
  		Table 3 Mean values for measures of Fusarium head blight resistance after artificial inoculation with Fusarium graminearum for two winter wheat genotypes

 
Despite large year-to-year variation in individual line response to FHB, differences in mean AUDPC and RWIS among RILs were consistent when lines were grouped according to alternative alleles at the marker loci (Table 4) . In all 3 yr, the lines carrying the GliR1 allele from Sincron (characteristic of the rye translocation T1BL.1RS) had a significantly lower AUDPC than lines with the GliB1b allele from F1054W. Similarly, the average AUDPC for lines with the GliD1b allele from Sincron was significantly lower than the average AUDPC of lines with GliD1g in 2 of the 3 yr and when averaged across years. None of the other marker genes showed any significant association with AUDPC (P > 0.05).


View this table:
[in this window]
[in a new window]
  		Table 4 Mean values for measures of Fusarium head blight resistance after artificial inoculation with Fusarium graminearum for recombinant inbred winter wheat lines grouped by parental allele of five marker loci

 
Association of marker loci with RWIS was similar to that observed for AUDPC (Table 4). In two of 3 yr and when averaged across years, lines with GliR1 had a significantly higher RWIS than lines with GliB1b. Inoculated spikes weighed an average of 23% more for lines with GliR1 than for lines with GliB1b. Lines carrying the allele GliD1b had a significantly higher RWIS than the lines withGliD1g in 1995, 1996 and for the three-year average. Overall, lines with GliD1b had a 14% higher weight of inoculated spikes than the GliD1g lines. Height-reducing genes and the W2 gene were not associated with FHB response.

The association between FHB resistance and gliadin loci GliB1 and GliD1 suggests that genes controlling response to Fusarium infection may be located on chromosomes T1BL.1RS and 1D. Chromosome 1B was previously found to be involved in the control of FHB resistance in Sumai 3 or its derivatives (Yu, 1982; Buerstmayr et al., 1997). Further research is needed to determine whether or not we located the same gene in a non-related wheat background or if we detected a different gene. There is only one previous report of a chromosome 1D effect on FHB resistance, and that was a negative effect on AUDPC in a set of Hobbit-sib [Triticum macha Dekapr. & Menabde] substitution lines (Grausgruber et al., 1997). Our results provide additional evidence that some T. aestivum genotypes might have favorable alleles for FHB resistance on chromosome 1D.

When the RILs were grouped according to the alleles at both GliB1 and GliD1 loci, gene effects were evidently cumulative, even though differences among the groups of lines were variable from year to year (Table 5) . However, for AUDPC, the effect of a favorable allele on one chromosome tended to be larger in the absence of the favorable allele on the other chromosome, and smaller if a favorable allele was already present on the other chromosome. For example, favorable alleles on chromosome T1BL.1RS reduced AUDPC on average by 140 units (74 in 1993–177 in 1996) in the absence of favorable alleles on chromosome 1D, but only by 95 units (65 in 1993–136 in 1995) when favorable allele(s) linked to GliD1b were present. A two-way analysis of variance showed significant interaction of the two loci in 1995, 1996, and for the average across years (data not shown). For RWIS, the interaction was significant only in 1996.


View this table:
[in this window]
[in a new window]
  		Table 5 Mean values for measures of Fusarium head blight resistance after artificial inoculation with Fusarium graminearum, for 102 recombinant inbred winter wheat lines grouped according to the alleles at GliB1 and GliD1 loci

 
Averaged over years, the QTL associated with the GliB1 locus accounted for 21% of the total variation of AUDPC among RILs and for 17% of the total variation of RWIS, while the QTL associated with the GliD1 locus only accounted for 7 and 9%, respectively. The average difference in AUDPC associated with the GliB1 locus was about 48% of the difference between the parents, while the difference associated with the GliD1 locus was about 26%. The average difference between lines with favorable alleles and lines with unfavorable alleles at both loci was only 58% of the difference between the parents. Obviously, other favorable QTL not associated with these two chromosomes were present in Sincron. On the other hand, compared with the resistant parent, we found mean AUDPC significantly lower in three RILs and mean RWIS higher one RIL. The presence of these transgressive segregants suggests that the susceptible parent F1054W may also have contributed resistance alleles.

If the cumulative effect of the two favorable QTL identified in our study is also present for other QTL, this would support the use of recurrent selection in breeding winter wheat for FHB resistance. Recurrent selection has proven effective in improving FHB resistance in spring wheat (Jiang et al., 1994). Our data suggest, however, that rate of gain in FHB resistance through recurrent selection will tend to decrease as favorable alleles accumulate. Frequency distributions for AUDPC and RWIS in the RILs grouped according to the alleles at both gliadin loci, show that, despite considerable overlapping, chances of selecting for higher FHB resistance are better in lines carrying both GliR1 and GliD1b than in those carrying only one or none of these alleles (Fig. 4 and 5) .



View larger version (21K):
[in this window]
[in a new window]
  		Fig. 4 Frequency distribution for the area-under-disease-progress curve (AUDPC) after artificial inoculation with Fusarium graminearum for 102 recombinant inbred winter wheat lines grouped according to alleles at GliB1 and GliD1 loci (averaged across 3 yr)

 


View larger version (22K):
[in this window]
[in a new window]
  		Fig. 5 Frequency distribution for relative weight of inoculated spikes (RWIS) after artificial inoculation with Fusarium graminearum for 102 recombinant inbred winter wheat lines grouped according to alleles at GliB1 and GliD1 loci (averaged across 3 yr)

 
Besides allowing the location on chromosomes T1BL.1RS and 1D of QTL affecting FHB resistance, the association between type II FHB resistance and alleles controlling specific gliadins may be useful to increase the frequency of resistant genotypes in segregating populations. For example, in this cross, discarding all segregants with GliB1b and GliD1g would eliminate all lines with AUDPC larger than 750, while retaining all lines with AUDPC smaller than 300. On the other hand, selecting only lines with both GliR1 andGliD1b would increase the frequency of lines with AUDPC smaller than 300 from 7.5 to over 18.5%. Obviously, selection for GliR1 would have a negative effect on bread-making quality (Dhaliwal et al., 1987). However, on the basis of the overlapping of AUDPC and RWIS distributions for lines with alternative alleles at the GliB1 locus, we suggest that the QTL for FHB resistance may not be on the translocated rye chromosome arm 1RS, where the GliR1 allele is located, but linked with it, rather loosely. Other parents might be found, which have the same QTL coupled with another allele of GliB1, more favorable for bread-making quality. On the other hand, identification of new molecular markers more closely linked with the QTL for FHB resistance on chromosome 1B, might allow selection for this QTL but against the presence of the GliR1 allele.

Received for publication April 22, 1998.


   REFERENCES
TOP
 ABSTRACT
 INTRODUCTION
 Materials and methods
 Results and discussion
 REFERENCES
 




This article has been cited by other articles:


Home page
 Crop Sci.Home page
J. Haberle, M. Schmolke, G. Schweizer, V. Korzun, E. Ebmeyer, G. Zimmermann, and L. Hartl
Effects of Two Major Fusarium Head Blight Resistance QTL Verified in a Winter Wheat Backcross Population
Crop Sci., September 1, 2007; 47(5): 1823 - 1831.
[Abstract] [Full Text] [PDF]

Home page
 Crop Sci.Home page
K. Semagn, H. Skinnes, A. Bjornstad, A. G. Maroy, and Y. Tarkegne
Quantitative Trait Loci Controlling Fusarium Head Blight Resistance and Low Deoxynivalenol Content in Hexaploid Wheat Population from 'Arina' and NK93604
Crop Sci., February 6, 2007; 47(1): 294 - 303.
[Abstract] [Full Text] [PDF]

Home page
 Crop Sci.Home page
X. Shen, M. Ittu, and H. W. Ohm
Quantitative Trait Loci Conditioning Resistance to Fusarium Head Blight in Wheat Line F201R
Crop Sci., May 1, 2003; 43(3): 850 - 857.
[Abstract] [Full Text] [PDF]

Home page
 Crop Sci.Home page
T. Miedaner, B. Schneider, and H. H. Geiger
Deoxynivalenol (DON) Content and Fusarium Head Blight Resistance in Segregating Populations of Winter Rye and Winter Wheat
Crop Sci., March 1, 2003; 43(2): 519 - 526.
[Abstract] [Full Text] [PDF]

Home page
 Agron. J.Home page
N. A. Slaton, S. D. Linscombe, R. J. Norman, and E. E. Gbur Jr.
Seeding Date Effect on Rice Grain Yields in Arkansas and Louisiana
Agron. J., January 1, 2003; 95(1): 218 - 223.
[Abstract] [Full Text] [PDF]

Home page
 Crop Sci.Home page
R. W. Stack, E. M. Elias, J. M. Fetch, J. D. Miller, and L. R. Joppa
Fusarium Head Blight Reaction of Langdon Durum-Triticum dicoccoides Chromosome Substitution Lines
Crop Sci., March 1, 2002; 42(2): 637 - 642.
[Abstract] [Full Text] [PDF]

This Article
Right arrow Abstract Freely available
Right arrow Figures Only
Right arrow Full Text (PDF) Free
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via ISI Web of Science (9)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Ittu, M.
Right arrow Articles by Mustãtea, P.
Right arrow Search for Related Content
PubMed
Right arrow Articles by Ittu, M.
Right arrow Articles by Mustãtea, P.
Agricola
Right arrow Articles by Ittu, M.
Right arrow Articles by Mustãtea, P.

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
The SCI Journals Agronomy Journal Vadose Zone Journal
Journal of Natural Resources
and Life Sciences Education		 Soil Science Society of America Journal
Journal of Plant Registrations Journal of
Environmental Quality		 The Plant Genome