Crop Science Journal of Natural Resources and Life Sciences Education
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Published online 1 March 2007
Published in Crop Sci 47:893-897 (2007)
© 2007 Crop Science Society of America
677 S. Segoe Rd., Madison, WI 53711 USA
This Article
Right arrow Abstract Freely available
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 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 Google Scholar
Google Scholar
Right arrow Articles by Oliver, R. E.
Right arrow Articles by Cai, X.
Right arrow Search for Related Content
PubMed
Right arrow Articles by Oliver, R. E.
Right arrow Articles by Cai, X.
Agricola
Right arrow Articles by Oliver, R. E.
Right arrow Articles by Cai, X.
Related Collections
Right arrow Plant Disease
Right arrow Plant Genetic Resources

PLANT GENETIC RESOURCES

Reaction of Wild Emmer Wheat Accessions to Fusarium Head Blight

R. E. Olivera, R. W. Stackb, J. D. Millerc and X. Caia,*

a Dep. of Plant Sciences, North Dakota State Univ., Fargo ND 58105
b Dep. of Plant Pathology, North Dakota State Univ., Fargo ND 58105
c USDA-ARS, Northern Crops Research Lab., Fargo, ND 58105

* Corresponding author (xiwen.cai{at}ndsu.edu).


   ABSTRACT
TOP
 NOTES
 ABSTRACT
INTRODUCTION
 MATERIALS AND METHODS
 RESULTS AND DISCUSSION
 REFERENCES
 
Fusarium head blight (FHB), caused mainly by Fusarium graminearum Schwabe, is a serious disease of wheat (Triticum spp.) worldwide. Host resistance has proven the most effective method of controlling FHB in common wheat (T. aestivum L., 2n = 6x = 42, genomes AABBDD). Progress in breeding for FHB resistance in durum wheat (T. turgidum L. ssp. durum, 2n = 4x = 28, genomes AABB), however, has been limited by a lack of resistance sources. Fortunately, durum wheat has a large number of tetraploid relatives, which represent a gene pool for improvement of FHB resistance in durum. The objective of this study was to search for sources of FHB resistance in wild emmer wheat [T. turgidum L. ssp. dicoccoides (Körn. ex Asch. & Graebner) Thell., 2n = 4x = 28, genomes AABB] (TDIC). We evaluated 416 accessions of wild emmer wheat for reaction to FHB using the point inoculation method in a greenhouse environment. Accessions exhibiting a low FHB disease rating in preliminary evaluations were retested in fully replicated experiments. Among the 416 accessions tested, there was wide variation in response to FHB, ranging from highly resistant to highly susceptible. Several accessions showed minimal disease development across two or more seasons and represent potential new sources to enhance resistance of durum wheat to FHB.

Abbreviations: FHB, Fusarium head blight • TDIC, Triticum turgidum L. ssp. dicoccoides.


   INTRODUCTION
TOP
 NOTES
 ABSTRACT
 INTRODUCTION
MATERIALS AND METHODS
 RESULTS AND DISCUSSION
 REFERENCES
 
FUSARIUM HEAD BLIGHT affects wheat and other small grains throughout the world. In the spring wheat-growing region of the North American Great Plains, FHB is caused mainly by F. graminearum (Stack and McMullen, 1985; Wilcoxson et al., 1988; Wong et al., 1992). Fortunately for plant breeding efforts, wheat genotypes resistant to F. graminearum are also resistant to the other Fusarium species (van Eeuwijk et al., 1995; Stack et al., 1997).

The degree of FHB infection is unpredictable and highly dependent on weather at the time of anthesis, when plants are most susceptible (Sutton, 1982). In the North American spring grain region, epidemics in 1993 and 1994 were very severe, with more moderate losses occurring from 1995 through 1998 (McMullen et al., 1997; Windels, 2000). Previous epidemics, on a more limited scale, occurred in the region during the 1980s (McMullen et al., 1997; Wilcoxson et al., 1988).

Recommended management practices, such as crop rotation or fungicide application, have not provided satisfactory control of the disease. Most researchers agree that incorporation of host plant resistance is the best long-term approach to limit losses due to FHB (Meidaner, 1997; Mesterhazy, 1997).

Resistance to FHB has been classified into five major types: (I) resistance to initial infection, (II) resistance to spread of infection within a spike, (III) decomposition or nonaccumulation of mycotoxins, (IV) resistance to kernel infection, and (V) yield tolerance (Schroeder and Christensen, 1963; Wang and Miller, 1988; Mesterhazy, 1995). Limited sources of resistance are available in hexaploid wheats, and these have been used in breeding programs (Rudd et al., 2001). However, a source of effective resistance to FHB has not been found in durum wheat, despite extensive efforts to identify resistance among the world collection of durum accessions. In addition, attempts to transfer FHB resistance from hexaploid wheat to durum have not been successful (E.M. Elias, personal communication, 2006).

Relatives of wheat have been used as a source of genetic variation for wheat improvement (Sears, 1972; Feldman and Sears, 1981; Jones et al., 1995) and resistance to FHB has been identified in a number of these relatives (Ban, 1997; Liu et al., 2000; Chen et al., 2001; Buerstmayr et al., 2003; Shen et al., 2004; Cai et al., 2005; Oliver et al., 2005). Tetraploid relatives (T. turgidium L. ssp. dicoccoides) of wheat that have the same genomes (AABB) as durum represent an important gene pool for durum improvement. Resistance to several diseases, including stem rust (Puccinia graminis Pers.) (Miller et al., 1998), stripe rust (P. striiformis Pers.) (Reinhold et al., 1983), leaf rust (P. triticina Eriks.) (Dyck and Bartos, 1994), and powdery mildew (Erysiphe graminis DC. f. sp. tritici Marchal) (Reader and Miller, 1991) were found in TDIC. In addition, preliminary work has suggested that TDIC may also be a potential source of FHB resistance (Miller et al., 1998). The objective of this research was to identify TDIC accessions with resistance to FHB, which might be used to enhance the FHB resistance in durum wheat.


   MATERIALS AND METHODS
TOP
 NOTES
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
RESULTS AND DISCUSSION
 REFERENCES
 
A total of 416 wild emmer accessions were screened in five experiments from 1995 through 2002. Seeds of those accessions were obtained from the National Plant Germplasm System, USDA-ARS, Aberdeen, ID. Three of these experiments (Spring 95, Spring 96, Spring 97) were extensive preliminary evaluations, designed to rate a large number of accessions and to eliminate obviously susceptible accessions. These tests used an augmented design with multiple repeated checks. To confirm the FHB response, the most resistant lines were reevaluated, using a randomized complete block design. To allow comparison of results between experiments, each experiment included a repeated set of TDIC accessions spanning the range of FHB response (PI 467019, PI 467023, PI 467026, PI 272582, PI 355459, PI 466995). The average infection of these accessions was used as a disease index. A durum cultivar with highest FHB resistance in the northern Great Plains, ‘Belzer’ (Elias et al., 1999), was also included as a resistant check, and a durum elite breeding line (D87450) served as a susceptible check.

Plant Culture
The TDIC accessions with a winter or semi-winter growth habit were vernalized at 4°C for 6 wk before being planted in the greenhouse. Plants were grown in the greenhouse at 20 to 25°C with supplemental lighting to increase daylength to 16 h.

Inoculum Preparation and Inoculation
Three strains of F. graminearum were used in all experiments. Each strain was cultured, maintained, and prepared separately, and spore suspensions of equal concentration were mixed together just before use. Strain R010 had been shown to be highly pathogenic in several previous experiments (Stack and McMullen, 1985; Stack, 1989). Strains R1267 and R1270 had been isolated from blighted wheat heads in eastern North Dakota and had been chosen for the ability to cause FHB (Stack and McMullen, 1985). All three cultures have consistently produced FHB symptoms in wheat (Stack et al., 1997, 2002a).

Inoculum preparation followed the methods of Stack (1989), using isolates of F. graminearum known from previous studies to be pathogenic. Before starting each experiment, each culture was freshly re-isolated from symptomatic inoculated plants. Cultures were grown on petri plates of carnation leaf agar or half-strength potato dextrose agar for 15 to 20 d at room temperature (22–24°C) under fluorescent lights. To prepare conidiospore inoculum, petri dish cultures were flooded with sterile distilled water and gently agitated; the resultant spore suspension was strained through several layers of sterile cheesecloth to remove hyphal fragments. The final concentration was adjusted to 50000 spores mL–1. Freshly prepared spore suspension was held on crushed ice and used within 4 h.

Inoculations were done using the single-spikelet method, in which a 10-µL droplet of spore suspension is placed into a single spikelet near the middle of each spike at anthesis. At the concentration used, each droplet contained approximately 500 conidiospores. This concentration was chosen to give maximum incidence while not overpowering any expression of resistance, if present (Stack, 1989). For the initial screening experiments, 10 spikes within each plant row were inoculated at mid to late anthesis. For the replicated experiments, three spikes per plant (27 spikes per line) were inoculated.

Following inoculation, plants were lightly misted and covered on three successive nights using a plastic tent to maintain high humidity after fogging. Plastic tents were removed during daylight hours to prevent overheating. After the third night, misting was stopped and the tents were permanently removed. At 3 to 3.5 wk post-inoculation, plants were evaluated for FHB and severity was scored on a percentage scale (Stack and McMullen, 1995). Disease incidence was also recorded as the percentage of inoculated heads showing symptoms.

Data Analysis
A separate analysis of variance was conducted on data for each season using the Statistical Analysis System version 9.1 (SAS Institute, Cary, NC). Where appropriate, mean separation was determined by Fisher's protected LSD at {propto} = 0.05 (Steel et al., 1997).


   RESULTS AND DISCUSSION
TOP
 NOTES
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS AND DISCUSSION
REFERENCES
 
One hundred and twenty-three accessions were evaluated in the Spring 95 greenhouse. Among these, nine accessions exhibited an FHB severity rating of 30% or less and a higher level of FHB resistance than Belzer, although not statistically significant (Table 1).


View this table:
[in this window]
[in a new window]

  		Table 1. Mean Fusarium head blight severity and incidence of wild emmer accessions.

 
In addition to the accessions evaluated in the Spring 95 greenhouse, 151 new accessions were evaluated in the Spring 96 greenhouse. As evidenced by the index, FHB infection was considerably higher in this season than in the previous (Table 1). Although a range of FHB severity was observed within the resistant lines, all repeated accessions and two newly evaluated accessions (PI 478742, PI 481521) were significantly more resistant than the susceptible checks. The same nine resistant accessions identified in the Spring 95 greenhouse exhibited significantly higher FHB severity than Belzer (Table 1). These results suggested that these nine accessions were more susceptible to FHB under the Spring 96 greenhouse environment than under the Spring 95 greenhouse environment. It has been previously shown that wheat genotypes respond differently to FHB under different environments (Stack, 2003).

Seven of the nine previously identified resistant accessions were reevaluated in the Fall 96 greenhouse. Again, a range of FHB response was observed, although all resistant accessions showed significantly less disease than the susceptible controls.

In the Spring 97 greenhouse, 142 accessions were evaluated for the first time. Sixteen accessions showed less than 30% FHB severity (Table 1). These 16 accessions, along with the previously identified five resistant accessions, were reevaluated in a replicated experiment (Spring 02) and exhibited FHB severity significantly lower than the susceptible controls and comparable to the resistant controls (Table 1). The mean FHB severity for each accession, however, was higher than in the Spring 97 greenhouse because of a higher disease index in this season (Table 1).

The TDIC accessions evaluated in each experiment exhibited a continuum of FHB response, with disease severity ranging from 8.8 to 100.0% and incidence from 67 to 100% (Table 1). In the two seasons with the highest disease index (Spring 96 and Spring 02), incidence was 100% in all accessions. Seventy-five accessions exhibited an intermediate FHB reaction (30 to 50% disease severity) (Table 2), and 312 accessions showed a disease severity greater than 50% (Tables 1 and 3).


View this table:
[in this window]
[in a new window]

  		Table 2. Wild emmer wheat accessions with an intermediate Fusarium head blight (FHB) reaction (30–50% disease severity).

 

View this table:
[in this window]
[in a new window]

  		Table 3. Wild emmer wheat accessions with a susceptible Fusarium head blight (FHB) reaction (>50% disease severity).

 
Wheat lines with high levels of FHB resistance generally possess multiple resistance genes, which act in an additive manner to confer resistance. Studies have shown that such genes, when present individually, confer only intermediate resistance (Waldron et al., 1999; Stack et al., 2002a, 2002b). Accessions exhibiting an intermediate reaction could have a minor gene(s) for resistance, thus preventing extreme susceptibility. An intermediate FHB reaction could also be caused by suppressor genes, which prevent expression of some FHB resistance genes (Stack et al., 2002a).

Reaction of wheat to FHB demonstrates a significant environmental effect (Stack, 2003). We observed significant variation for expression of disease severity within some resistant accessions across seasons, indicating that reaction of those accessions to FHB is highly dependent on the environment. Multiple factors are involved in FHB development, some of which may not yet be identified. Two accessions (PI 478742, PI 481521) demonstrated consistently high resistance across four seasons, two of which had a high disease index (Table 1). Since minimal disease development was observed under all four environments, these accessions could be particularly useful sources of FHB resistance.

The TDIC accessions identified as resistant to FHB in this study have different geographical origins (Table 1) and may represent diverse sources of FHB resistance. Resistance genes in these accessions should be transferable to durum wheat genomes via homologous recombination because both TDIC and durum wheat have the same genomes (AABB). Since a source of effective FHB resistance has not been available for durum, these resistant TDIC accessions could be used to develop resistance to FHB in durum wheat.

Two TDIC accessions, Israel A and PI 481521, were identified to contain FHB resistance genes in previous studies (Stack et al., 2002a, 2003). A major FHB resistance QTL was detected on chromosome 3A in Israel A (Otto et al., 2002) and has been utilized in durum breeding (E.M. Elias, personal communication, 2006). Expression of this QTL has been demonstrated in synthetic hexaploid wheat (Berzonsky et al., 2004; Hartel et al., 2004). Although Israel A per se is susceptible to FHB (Table 1; Stack et al., 2002a), the FHB resistance QTL on chromosome 3A is probably suppressed by one or more other genes present in the genomes of Israel A. Other research suggests that the suppressor gene is located on chromosome 2A (Stack et al., 2002a; Garvin et al., 2003).

Two sets of chromosome substitution lines, with one pair of TDIC chromosomes substituting for the homologous chromosome pair of the durum wheat cultivar Langdon (LDN), were developed using PI 478742 and PI 481521, two FHB resistant accessions of T. turgidum L. ssp. dicoccoides (Table 1; Xu et al., 2004). They were designated as "LDN-DIC(742)" and "LDN-DIC(521)," respectively (GrainGenes, 2006; Joppa et al., 1997; Stack et al., 2002a, 2002b). Evaluation of FHB reaction in LDN-DIC(742) lines showed significantly reduced disease in the substitution lines involving chromosomes 7A and 7B. These two chromosomes, therefore, were proposed to carry FHB resistance genes in this wild emmer accession (Stack et al., 2002b). Screening of the LDN-DIC(521) lines indicated that chromosome 1A, 3A, 5B, and 7A may carry resistance genes (Stack et al., 2003). As yet unreported, FHB resistance genes could be found in other resistant TDIC accessions.

Direct utilization of the resistant TDIC accessions in durum breeding may be problematic due to various undesirable traits, including late maturity, shattering, and unfavorable end-use quality, although these accessions share genomes and have a high cross-compatibility with durum. These materials, therefore, require a "pre-breeding" phase. By eliminating unfavorable characteristics, breeder-friendly germplasm could be developed, allowing deployment of FHB resistance from T. dicoccoides to durum wheat cultivars.


   ACKNOWLEDGMENTS
 
The authors thank Dr. L.R. Joppa for providing seeds for the TDIC accessions and Drs. Justin Faris and William Berzonsky for critical review of the manuscript. We also thank Jana Hansen, Jennifer Mitchell Fetch, and Mary E. Johnshoy for technical assistance.


   NOTES
TOP
 NOTES
ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS AND DISCUSSION
 REFERENCES
 
All rights reserved. No part of this periodical may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, or any information storage and retrieval system, without permission in writing from the publisher. Permission for printing and for reprinting the material contained herein has been obtained by the publisher.

Received for publication August 18, 2006.


   REFERENCES
TOP
 NOTES
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS AND DISCUSSION
 REFERENCES
 





This Article
Right arrow Abstract Freely available
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 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 Google Scholar
Google Scholar
Right arrow Articles by Oliver, R. E.
Right arrow Articles by Cai, X.
Right arrow Search for Related Content
PubMed
Right arrow Articles by Oliver, R. E.
Right arrow Articles by Cai, X.
Agricola
Right arrow Articles by Oliver, R. E.
Right arrow Articles by Cai, X.
Related Collections
Right arrow Plant Disease
Right arrow Plant Genetic Resources

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