Genetic studies of fusarium head blight resistance in the winter wheat cultivar Ernie.

摘要

Fusarium head blight (FHB), also called scab, mainly caused by the fungus Fusarium graminearum Schwabe [telomorph: Gibberella zeae Schw. (Petch)], is a serious disease that affects wheat ( Triticum aestivum L. and T. durum L.) and barley (Hordeum vulgare L.) in warm, humid areas of the world. Yield losses in the United States during the 1990s were close to {dollar}3.0 billion. Genetic resistance is the most effective and economical solution to the yield and quality losses, however, breeding is hindered by a lack of resistance genes. Current genetic studies and breeding programs are focusing on the Chinese cultivar ‘Sumai 3’ and its derivatives. ‘Ernie’, a soft red winter wheat cultivar, was released from the Missouri Agricultural Experiment Station in 1995. It has a high level of FHB resistance, yet the genetics of its resistance are not well understood. This research was designed to study the genetics of FHB resistance in Ernie through both molecular and conventional approaches. A set of 244 F₈ recombinant inbred lines were developed from the cross Ernie/MO 94-317. Four assessments of type II FHB resistance including spread, spread with wilt, the Fusarium head blight index (FHBI), and FHBI with wilt were made. All were highly significantly correlated with coefficients ranging from 0.699** to 0.915**. The number of effective factors for FHB resistance in Ernie was estimated as two for spread and four for FHBI. Five QTLs were identified on five different chromosomes (2B, 3B, 4BL, 5A, and 5DL) which were linked to FHBI and FHBI with wilt. The QTLs with larger effects for FHB resistance were on chromosomes 4BL, 5A, and 5DL and explained 10 to 33% of the phenotypic variation. The QTL on 5A was also associated with disease spread and spread with wilt and explained 10 to 12% of the phenotypic variation. All FHB resistant alleles were from Ernie. Multiple regression indicated that these five QTLs explained 36 to 37% of the phenotypic variation for FHBI and FHBI with wilt, respectively. Significant interactions between markers were included in the model and explained 53.8% and 43.2% of the total variation for these two traits, respectively. Based on the chromosome locations, linked markers, and the magnitude of their effects, the QTLs in Ernie differ from those in Sumai 3. Three QTLs for days to flower were identified on chromosomes 2A, 2DS, and 5B. The major QTL on 2DS explained 61.9% of the phenotypic variation. One QTL was also detected on 5AL for absence of awns. The major QTL on 2DS was common between days to flower and spike length; however, neither was common with QTLs for FHB resistance.; Generation mean and variance analyses were done on six generations including the parents, F₁ (Ernie/MO 94-317), BC₁ (F₁/Ernie), BC₂ (F₁/MO 94-317), and the F₂. Additive effects were the major effects for both spread and FHBI. Broad-sense heritability estimates for the F₂ were 78.2% and 78.3% for spread and FHBI, respectively, while the narrow-sense heritabilities were 51.3% and 55.4%, respectively. Because of the additivity of these genetic effects, we concluded that pyramiding the genes from Ernie with those from other sources of resistance should enhance the level of FHB resistance in wheat.