Plant pathogenic fungi represent the largest group of disease-causing agents on crop plants, and are a constant and major threat to agriculture worldwide. Recent studies have shown that engineered production of RNA interference (RNAi)-inducing dsRNA in host plants can trigger specific fungal gene silencing and confer resistance to fungal pathogens. Although these findings illustrate efficient uptake of host RNAi triggers by pathogenic fungi, it is unknown whether or not such an uptake mechanism has been evolved for a natural biological function in fungus-host interactions. Here, we show that in response to infection with Verticillium dahliae (a vascular fungal pathogen responsible for devastating wilt diseases in many crops) cotton plants increase production of microRNA 166 (miR166) and miR159 and export both to the fungal hyphae for specific silencing. We found that two V. dahliae genes encoding a Ca-dependent cysteine protease (Clp-1) and an isotrichodermin C-15 hydroxylase (HiC-15), and targeted by miR166 and miR159, respectively, are both essential for fungal virulence. Notably, V. dahliae strains expressing either Clp-1 or HiC-15 rendered resistant to the respective miRNA exhibited drastically enhanced virulence in cotton plants. Together, our findings identify a novel defence strategy of host plants by exporting specific miRNAs to induce cross-kingdom gene silencing in pathogenic fungi and confer disease resistance.
SUMMARYRapid progress has been made regarding the understanding of brassinosteroid (BR) signaling in Arabidopsis. However, little is known about BR signaling in monotyledons. Here, we characterized a rice dwarf and lowtillering (dlt) mutant and cloned the corresponding gene via map-based cloning. DLT encodes a new member of the plant-specific GRAS family. The dwarf phenotype of dlt is similar to BR-deficient or signaling mutants in rice. In addition, both lamina bending and coleoptile elongation assays show that dlt is insensitive or much less responsive to brassinolide (BL), the most active BR, suggesting that DLT is involved in BR signaling. Consistent with this conclusion, the accumulation of transcripts of BR biosynthesis genes in the dlt mutant indicated that DLT is involved in feedback inhibition of BR biosynthesis genes. In addition, transcription of several other BRregulated genes is altered in the dlt mutant. Finally, consistent with the fact that DLT is also negatively feedback-regulated by BR treatment, a gel mobility shift assay showed that OsBZR1 can bind to the DLT promoter through the BR-response element. Taken together, these studies have enabled us to identify a new signaling component that is involved in several specific BR responses in rice.
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