Abstract
Fusarium head blight (FHB) and sharp eyespot are important diseases of the cereal plants, including bread wheat (Triticum aestivum) and barley. Both diseases are predominately caused by the pathogenic fungi, Fusarium graminearum and Rhizoctonia cerealis. The roles of the wheat-wall-associated kinases (WAKs) in defense against both F. graminearum and R. cerealis have remained largely unknown. This research reports the identification of TaWAK2A-800, a wheat WAK-coding gene located on chromosome 2A, and its functional roles in wheat resistance responses to FHB and sharp eyespot. TaWAK2A-800 transcript abundance was elevated by the early infection of R. cerealis and F. graminearum, or treatment with exogenous chitin. The gene transcript seemed to correspond to the resistance of wheat. Further functional analyses showed that silencing TaWAK2A-800 compromised the resistance of wheat to both FHB (F. graminearum) and sharp eyespot (R. cerealis). Moreover, the silencing reduced the expression levels of six defense-related genes, including the chitin-triggering immune pathway-marker genes, TaCERK1, TaRLCK1B, and TaMPK3. Summarily, TaWAK2A-800 participates positively in the resistance responses to both F. graminearum and R. cerealis, possibly through a chitin-induced pathway in wheat. TaWAK2A-800 will be useful for breeding wheat varieties with resistance to both FHB and sharp eyespot.
Highlights
Bread wheat (Triticum aestivum) is one of the most important staple food crops in the world
This study reveals the function of TaWAK2A-800 in the broad-spectrum resistance of wheat to both sharp eyespot by R. cerealis, and Fusarium head blight (FHB) by F. graminearum
In two batches of virus-induced gene-silencing (VIGS) and disease scoring at 35 dpi with the pathogen, R. cerealis WK207, the average infection types (ITs) on the stems of the TaWAK2A-800-silenced wheat cultivar CI12633 plants were between 2.50 and 2.89 (Figure 4F), while those of the BSMV:GFP-infected CI12633 plants were 1.71 to 1.93, respectively. These results indicate that knocking-down TaWAK2A-800 in the wheat cultivar, CI12633, could cause higher susceptibility to the pathogen R. cerealis, and suggests that TaWAK2A-800 was required for wheat-resistance responses against pathogenic R. cerealis infection
Summary
Bread wheat (Triticum aestivum) is one of the most important staple food crops in the world. Wheat production is threatened in many areas by devastating pests and pathogens [1]. Rhizoctonia cerealis is a necrotrophic fungal pathogen responsible for the sharp eyespot, which is a devastating disease of wheat and other cereal plants in some countries of the world, especially in China [5,6]. The breeding of disease-resistant wheat varieties is the most environmentally sustainable and effective strategy for minimizing the losses caused by FHB and sharp eyespot. Traditional resistance breeding is challenging since there are no wheat cultivars with full resistance to FHB or sharp eyespot [7,8]. To improve wheat resistance to F. graminearum and R. cerealis, it is important to isolate the pivotal resistance QTL/genes
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