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Targeting the pattern-triggered immunity pathway for enhancing resistance to Fusarium graminearum.

Molecular Plant Pathology 2018 December 31
FHB (Fusarium head blight) is a disease of the floral tissues of wheat and barley for which highly resistant varieties are not available, thus necessitating the need for identifying genes/mechanisms that can be targeted for controlling this devastating disease. Fusarium graminearum is the primary causal agent of FHB in North America. In addition, it also causes Fusarium seedling blight. F. graminearum can also cause disease in the model plant Arabidopsis thaliana. The Arabidopsis-F. graminearum pathosystem has facilitated the identification of targets for controlling disease caused by this fungus. Here we show that resistance against F. graminearum can be enhanced by flg22, a bacterial MAMP (microbe-associated molecular pattern). Flg22-induced resistance in Arabidopsis required its cognate PRR (pattern recognition receptor) FLS2, and was accompanied by the upregulation of WRKY29. Expression of WRKY29, which is associated with PTI (pattern-triggered immunity), was also induced in response to F. graminearum infection. Furthermore, WRKY29 was required for basal resistance as well as flg22-induced resistance to F. graminearum. Conversely, constitutive expression of WRKY29 in Arabidopsis enhanced disease resistance. The PTI pathway is also activated in response to F. graminearum infection of wheat. Furthermore, flg22 application and ectopic expression of WRKY29 enhanced FHB resistance in wheat. Thus, we conclude that the PTI pathway provides a target for controlling FHB in wheat. We further show that ectopic expression of WRKY29 in wheat results in shorter stature and early heading time, both traits that are important to wheat breeding. This article is protected by copyright. All rights reserved.

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