Antagonism between SUMO1/2 and SUMO3 regulates SUMO conjugate levels and fine-tunes immunity.

Attachment of SMALL UBIQUITIN-LIKE MODIFIER (SUMO) on target proteins regulates a plethora of cellular processes across eukaryotes. In Arabidopsis thaliana, mutants with abnormal SUMO1/2 conjugate levels display for example a dwarf stature, auto-immunity, and altered stress responses to adverse environmental conditions. Since the SUMO pathway is known to autoregulate its biochemical activity (via allosteric interactions), we here assessed whether the emergence of additional SUMO paralogues in Arabidopsis has introduced the capacity of self-regulation by means of isoform diversification in this model plant. By studying the plant defense responses elicited by the bacterial pathogen Pseudomonas syringae pv. tomato, we now provide genetic evidence that SUM3, a divergent paralogue, acts downstream of the two main SUMO paralogues, SUM1/2. Expression of SUM3 apparently buffers or suppresses the role of SUM1/2 by controlling the timing and amplitude of the immune response. Moreover, SUM1 and SUM2 work additively to suppress both basal and TNL-specific immunity, a specific branch of the immune network. Finally, our data reveal that SUM3 is required for the global increase in SUMO1/2 conjugates upon exposure to (a)biotic stresses, i.e. heat and pathogen exposure. We cannot exclude that this latter effect is independent of the former role of SUM3 on immunity.