Contrasting functions of Arabidopsis SUMO1/2 isoforms with SUMO3 intersect to modulate innate immunity and global SUMOylome responses

Reversible covalent attachment of SMALL UBIQUITIN-LIKE MODIFIERS (SUMOs) on target proteins regulate diverse cellular process across all eukaryotes. In Arabidopsis thaliana, most mutants with perturbed SUMOylation display severe impairments in growth and adaptations to physiological stresses. Since SUMOs self-regulate SUMOylation efficiencies, existence of multiple isoforms introduces possibilities of their functional intersections which remain unexplored. Using well-established defense responses elicited against virulent and avirulent Pseudomonas syringae pv. tomato strains, we investigated crosstalks in individual and combinatorial Arabidopsis sum mutants. We report that while SUM1 and SUM2 additively, but not equivalently suppress basal and TNL-specific immunity, SUM3 promotes these defenses. Remarkably, the loss of SUM3 partially attenuates heightened immunity of sum1 or sum2 mutants suggesting intricate crosstalks among these isoforms in optimizing immune amplitudes. Similar SUM1-SUM3 intersections also affect global SUMOylome responses to heat-shock. Overall, our investigations reveal novel insights into auto-regulatory mechanisms of host SUMOylome maintenance and adjustments to environmental challenges.