(Submitter supplied) Plants integrate endogenous and environmental signals to regulate growth and developmental programs by the use different hormonal pathways. Perception of Pathogen/Microbial Associated Molecular Patterns (PAMPs/MAMPs) from invading microorganisms triggers a series of defense reactions known as Pathogen Triggered Immunity (PTI) that inhibit growth promoting signaling pathways such as auxin signaling. On the contrary, pathogens manipulate growth signaling and metabolism to promote disease susceptibility, but how this hormone acts on immunity is not fully understood. Ustilago maydis is a fungal pathogen of maize. Infected plants show formation of galls, masses of undifferentiated tissue, and upregulation of auxin signaling. Here we show that a secreted protein from U. maydis, the effector Naked1 (Nkd1), translocates into the host nucleus where it interacts with members of the Topless/Topless related family of transcriptional co-repressors. Nkd1 binds to TPL/TPRs through its native EAR motif and prevents recruitment of transcriptional repressors involved in hormonal signaling, leading to the de-repression of jasmonic acid and auxin responsive genes. We show that up-regulation of auxin signaling leads to inhibition of PAMP-triggered ROS burst, one of the earliest PTI responses, and increased susceptibility to pathogens. Thus, establishing a clear mechanism for auxin-induced pathogen susceptibility. Using engineered variants of Nkd1, with altered affinity/specificity to TPL/TPRs, we show that increased EAR-mediated binding triggers typical salicylic acid mediated defense reactions, leading to pathogen resistance.
- Organism:
- Arabidopsis thaliana
- Type:
- Expression profiling by high throughput sequencing
- Platform:
- GPL19580
- 24 Samples
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