H 2 O 2 sulfenylates CHE linking local infection to establishment of systemic acquired resistance
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Abstract
In plants, a local infection can lead to systemic acquired resistance (SAR) through increased production of salicylic acid (SA). For 30 years, the identity of the mobile signal and its direct transduction mechanism for systemic SA synthesis in initiating SAR have been hotly debated. We found that, upon pathogen challenge, the cysteine residue of transcription factor CHE undergoes sulfenylation in systemic tissues, enhancing its binding to the promoter of SA-synthesis gene, ICS1 , and increasing SA production. This occurs independently of previously reported pipecolic acid (Pip) signal. Instead, H 2 O 2 produced by NADPH oxidase, RBOHD, is the mobile signal that sulfenylates CHE in a concentration-dependent manner. This modification serves as a molecular switch that activates CHE-mediated SA-increase and subsequent Pip-accumulation in systemic tissues to synergistically induce SAR.
One Sentence Summary
RBOHD-generated H 2 O 2 sulfenylates transcription factor CHE to establish systemic acquired resistance in plants.
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Excerpt
30-years of searching for the link between local infection and systemic acquired resistance: It’s been ROS all along!
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