Phosphorylation of KAT-2B by WKS1/Yr36 redirects the lipid flux to jasmonates to enhance resistance against wheat stripe rust

Abstract

Wheat (Triticum aestivum) is one of the most essential human energy and protein sources. However, wheat production is threatened by devastating fungal diseases such as stripe rust, caused by Puccinia striiformis Westend. f. sp. tritici (Pst). Here, we reveal that the alternations in chloroplast lipid profiles and the accumulation of jasmonate (JA) in the necrosis region activate JA signaling and trigger the host defense. The collapse of chloroplasts in the necrosis region results in accumulations of polyunsaturated membrane lipids and the lipid-derived phytohormone JA in transgenic lines of Yr36 that encodes Wheat Kinase START 1 (WKS1), a high-temperature-dependent adult plant resistance protein. WKS1.1, a protein encoded by a full-length splicing variant of WKS1, phosphorylates and enhances the activity of keto-acyl thiolase (KAT-2B), a critical enzyme catalyzing the β-oxidation reaction in JA biosynthesis. The premature stop mutant, kat-2b, accumulates less JA and shows defects in the host defense against Pst. Conversely, overexpression of KAT-2B results in a higher level of JA and limits the growth of Pst. Moreover, JA inhibits the growth and reduces pustule densities of Pst. This study illustrates the WKS1.1‒KAT-2B‒JA pathway for enhancing wheat defense against fungal pathogens to attenuate yield loss.