Understanding the basis of resistance to Fusarium head blight in UK winter wheat

Summary

Sector:
Cereals & Oilseeds
Project code:
PR432
Date:
01 April 2003 - 31 March 2007
Funders:
AHDB Cereals & Oilseeds.
AHDB sector cost:
£225,579 From HGCA (Project No. 2726)
Total project value:
£537,869
Project leader:
P. Nicholson1 , R. Bayles2 and P. Jennings3 1 John Innes Centre, Norwich Research Park, Colney, Norwich NR4 7UH 2 NIAB, Huntingdon Road, Cambridge CB3 0LE 3 Central Science Laboratory, Sand Hutton, York, YO41 1LZ

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About this project

Abstract

Fusarium head blight (FHB) of wheat is caused predominantly by Fusarium graminearum and F. culmorumalthough other Fusarium species and Microdochium majus and M. nivale are also important in some regions. The disease can often contaminate the grain with mycotoxins such as deoxynivalenol (DON) and nivalenol (NIV). Of 53 UK National List varieties tested for response to FHB, only three (Soissons, Spark and Vector) had significant stable resistance over trials. UK barley varieties differed significantly in FHB resistance.

Three FHB resistant varieties were studied to identify the location of quantitative trait loci (QTL) associated with FHB resistance. Analysis of Spark and Soissons was combined with study of near-isogenic semi-dwarf lines for Rht1 and Rht2. Our results demonstrated that Rht2 is associated with a significant increase in susceptibility to initial infection (Type I resistance) while being largely unaffected in resistance to spread within the spike (Type II resistance). In contrast, Rht1 conferred no negative effect on FHB resistance, even conferring a very minor positive effect in one trial. Under high disease pressure both Rht1and Rht2 significantly decreased Type 1 resistance. However, while Rht2 had no effect on Type 2 resistance Rht1 significantly increased Type 2 resistance. Enhanced susceptibility associated with Rht2 is probably due to linkage to deleterious genes rather than to pleiotropy and the positive effect of Rht1 on FHB resistance is due either to pleiotropy conferring Type 2 resistance or very tight linkage to resistance genes. In the third variety (RL4137), we identified FHB resistance QTL on chromosomes 1B and 2B.

Correlation for resistance to F. culmorum (DON-producer) and M. majus (non toxin-producer) was moderate across 29 European varieties following spray inoculation. Following point inoculation M. majuswas not able to spread. Type 2 resistance appears to be important to restrict spread of DON-producing isolates of some species but may be largely irrelevant for other pathogens. Spread of a NIV-producing isolate of F. graminearum was much slower than that of a DON producing isolate. These isolates were used to identify and characterise new sources of FHB resistance among 300 lines from CIMMYT. 60 lines were shown to have moderate/high levels of FHB resistance. A few lines possessed a high level of Type I resistance only whereas a greater number possessed both Type I and Type II resistance. These lines merit further study as potential sources of novel FHB resistance. Furthermore, we propose that spray inoculation with an appropriate aggressive non DON-producing FHB pathogens may be used to identify the Type I FHB resistance component in wheat.

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