3.4.10
RESISTANCE TO INITIAL INFECTION AND COLONIZATION BY FUSARIUM EAR BLIGHT IN WINTER WHEAT

AJ HILTON1, P JENKINSON1, TW HOLLINS 2 and DW PARRY3

1Crop and Environment Research Centre, Harper Adams Agricultural College, Newport, Shropshire TF108NB, UK; 2Plant Breeding International, Maris Lane, Trumpington, Cambridge, CB22LQ, UK; 3HRI East Malling, West Malling, Kent ME196BJ, UK

Background and objectives
Fusarium ear blight (FEB) is caused by a range of pathogens including Fusarium culmorum, F. graminearum, F. avenaceum, F. poae and Microdochium nivale. Infection of ears by these pathogens following rainfall at anthesis can result in a reduction in grain yield and contamination with mycotoxins. Although most genotypes are susceptible to FEB, in the field, some genotypes have limited resistance with at least two factors being involved. These include resistance to initial infection at anthesis (Type I) and resistance to spread of infection within the ear (Type II) [1]. The aim of this study was to examine factors which could explain differences between cultivars in Type I and II resistance.

Materials and methods
In order to determine the basis of Type I resistance the effect of anthers collected from five winter wheat cultivars on percentage germination, total germ-tube length (mm) and germ-tube branching of F. culmorum conidia was investigated. In each experiment ten single anthers from each cultivar were placed into separate Eppendorff tubes containing 10 l of conidial suspension of F. culmorum (100,000 spores/ml). After 5 h incubation in darkness at 20C the incidence of conidial germination was assessed and after 12 h total germ-tube length was measured and the number of terminal points recorded as a measure of germ-tube branching. Results obtained were compared with control treatments where anthers were absent.

To understand the basis of Type II resistance, individual spikelets were inoculated on 20 replicate ears of 12 winter wheat cultivars, by introducing 25 l of a conidial suspension of F. culmorum (250,000 spores/ml) between the lemma and palea of the tenth spikelet from the base of the ear at GS 65. Twenty eight days after inoculation, the number of spikelets showing necrosis and scalding (premature bleaching above the point of inoculation) was recorded for each ear.

Results and conclusions
Anthers from all wheat cultivars tested significantly (P<0.001) increased the incidence of conidial germination (%), and total germ-tube length of F. culmorum conidia compared to controls; there were no significant differences between cultivars. Anthers from all wheat cultivars also significantly (P<0.001) increased germ-tube branching compared to the control and there were significant (P<0.05) differences between cultivars. For example, conidia, in the presence of anthers from Mercia and Beaver had a higher percentage of germ-tubes with four terminal points (14 and 13%) compared with Riband and Hussar (6 and 4%). This compares with the percentage of conidia with two germ-tubes which was greater in the presence of anthers from Riband and Hussar (58 and 59%) than Mercia and Beaver (41 and 44%). As a rise in the number of terminal points may be regarded as an increase in the number of potential infection sites, it is proposed that Mercia and Beaver are more susceptible to initial infection than Hussar and Riband.

Cultivars also differed significantly (P<0.01) in the percentage of spikelets showing necrosis and scalding following point inoculation of individual spikelets. In resistant cultivars such as Apollo, necrosis was often restricted to the inoculated spikelet, but in more susceptible cultivars, such as Beaver and Riband, necrosis spread down the ear affecting up to four and six spikelets respectively. Regression analysis revealed that a rise in the incidence of necrotic spikelets significantly increased the number of scalded spikelets (R2=0.34).

Since those cultivars exhibiting good resistance to initial infection did not necessarily exhibit good resistance to colonisation of ears it is proposed that both Type I and Type II resistance play an important role in cultivar resistance to FEB.

References
1. Schroeder HW, Christensen JJ, 1963. Phytopathology 53, 831-8.