Abstract
Wheat powdery mildew disease caused by the obligate biotrophic fungal pathogen Blumeria graminis forma specialis tritici (B.g. tritici) seriously threatens global wheat production. Although improved powdery mildew resistance is an aim in wheat breeding, the regulatory mechanism underlying the wheat-B.g. tritici interaction remains poorly understood. In this study, the wheat chromatin remodeling protein TaSWP73 was identified as a negative regulator of post-penetration resistance against B.g. tritici. The transient overexpression of TaSWP73 attenuates wheat post-penetration resistance against B.g. tritici, while the silencing of TaSWP73 potentiates salicylic acid (SA) biosynthesis and activates post-penetration resistance against B.g. tritici. Importantly, chromatin in the promoter regions of TaSARD1, an activator gene of SA biosynthesis, is marked by high nucleosome occupancy in the TaSWP73-silenced wheat leaves. The silencing of TaSARD1 could suppress SA biosynthesis and attenuate post-penetration resistance against B.g. tritici with a lack of TaSWP73. In addition, TaICS1 was characterized as an essential component of wheat SA biosynthetic machinery. Potentiated SA biosynthesis and increased post-penetration resistance against B.g. tritici with a lack of TaSWP73 could be suppressed by the silencing of TaICS1 expression. These results collectively support the hypothesis that the wheat chromatin remodeling protein TaSWP73 contributes to the compatible wheat-powdery mildew interaction presumably via the suppression of the TaSARD1-TaICS1-SA pathway.