Cross-species variations of cis-regulatory mechanisms of salicylic acid biosynthesis and systemic acquired resistance in plants.

Synthase 1 (ICS1) in distal tissues following a local pathogen infection.While the molecular mechanisms of SAR have been extensively characterized in Arabidopsis, their regulation across diverse plant species remains largely unexplored.In this study, we demonstrate that the CHE-ICS1 regulatory module is not universally conserved across plants.We identified natural variation in the cis-element within ICS1 promoters that affects CHE binding to ICS1.Even among Brassicaceae species, where the ICS1 pathway is the primary route for SA biosynthesis rather than the phenylalanine ammonia-lyase (PAL) pathway, variation in the ICS1 promoter affects the CHE-ICS1 interaction, resulting in its loss in some species.Notably, the Brassicaceae species lacking a functional CHE-ICS1 interaction fail to induce systemic ICS1 expression and SA accumulation in response to pathogen infection.Nevertheless, SAR still occurs in these species, albeit at reduced levels compared to Arabidopsis, suggesting the presence of SA-independent signaling pathways.Our findings demonstrate that cis-regulatory variation in the ICS1promoter contributes to interspecies divergence in SAR mechanisms, highlighting the evolutionary flexibility of plant immune regulation.1. Origin of CHE and its sequence conservation across plants 2. Variation in TCP binding sites within ICS1 promoters 3. Impacts of variation in TCP site on CHE binding to ICS1 promoters 4. ICS1 induction and SA accumulation correlated with variation in TCP site