The cysteine-rich receptor-like kinase TaCRK3 contributes to defense against Rhizoctonia cerealis in wheat.

Sharp eyespot, caused by the necrotrophic fungal pathogen Rhizoctonia cerealis, is a devastating disease of bread wheat (Triticum aestivum). However, the molecular mechanisms underlying wheat defense against R. cerealis are still largely unknown. In this study, by comparative transcriptomic analysis we identified a novel cysteine-rich receptor-like kinase (CRK)-encoding gene, designated as TaCRK3, and investigated its role in defense against R. cerealis. TaCRK3 transcript abundance was significantly elevated by R. cerealis and exogenous ethylene treatments. Silencing of TaCRK3 significantly compromised resistance to R. cerealis and repressed expression of an ethylene biosynthesis enzyme-encoding gene, ACO2, and a subset of defense-associated genes in wheat, whose transcript levels are up-regulated by ethylene stimulus. TaCRK3 protein was localized at the plasma membrane in wheat. Noticeably, both the heterologously expressed TaCRK3 protein and its partial peptide harboring two DUF26 (DOMAIN OF UNKNOWN FUNCTION 26) domains could inhibit growth of R. cerealis mycelia. These results suggest that TaCRK3 mediates wheat resistance to R. cerealis through direct antifungal activity and heightening the expression of defense-associated genes in the ethylene signaling pathway. Moreover, its DUF26 domains are required for the antifungal activity of TaCRK3. Our results reveal that TaCRK3 is a promising gene for breeding wheat varieties with resistance to R. cerealis.
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