P-400 - Immune regulators CBP60g and SARD1 modulate salt tolerance responses and mitigate the impact of combined pathogen-salt stress

Plants constantly navigate multiple stressors that challenge both survival and immunity. My research demonstrates that the immune regulator CBP60g is not only involved in defense pathways, but could also confer salt stress tolerance, and increased disease resilience to Pseudomonas syringae DC3000 (Pst DC3000) under salt stress. Overexpression of CBP60g using 35S::CBP60g, rescues the SA pathway inhibited under salt stress, suggesting a protective role of CBP60g under saline conditions.
Effector translocation assays reveal that Pst DC3000 virulence increases under salt stress in Col-0, but not in 35S::CBP60g, which could imply that CBP60g also limits bacterial invasion. Additionally, Pst DC3000 carrying the proU osmotic stress reporter senses osmotic stress in Col-0 under salt but not in 35S::CBP60g, indicating altered apoplastic conditions. Ion content analysis further shows that 35S::CBP60g plants maintain a lower Na⁺/K⁺ ratio than Col-0, which may contribute to salt tolerance. This indicates a more complex role of CBP60g, not only in response to pathogen infection but salt stress alone, potentially by modifying the apoplastic environment. 
Through transcriptomic, metabolomic, and microbiome analyses, I investigate how CBP60g influences host defense and apoplastic dynamics under salt stress. By integrating LC-MS/MS, RNA-seq, ICP-MS, 16S rRNA sequencing, and bacterial fitness assays, my findings reveal CBP60g’s key role in shaping plant immunity and salt stress adaptation.