Autoimmunity in camta3 is triggered by NLR immune receptors 
S. LOLLE (1), C. Greeff (1), M. Roux (1), K. Sømark (1), J. Mundy (1), M. Petersen (1) (1) Department of Biology, University of Copenhagen, Denmark

To evade recognition and support their growth pathogens deploy effectors into host cells to modify or remove host proteins. Plants can detect these effector mediated changes via Resistance proteins (NLRs). A model thus proposes that NLRs ‘guard’ host ‘guardees’. A corollary to this model is that forms of plant autoimmunity are due to inappropriate NLR activation. We have found that NLR triggered immunity can be prevented by the expression of dominant negative (DN) NLR forms. This DN approach is faster than crossing in knock-outs, and has the advantage of ‘poisoning’ redundant genes due to NLR homo- and hetero-dimerization. To exploit this, we did a large-scale screen for suppressors of autoimmunity in Arabidopsis and found that camta3 autoimmunity is suppressed by the expression of DN versions of two different NLRs, Dominant Suppressor of CAMTA3 (DSC) 1 & 2. EDS1 levels are elevated in camta3 and CAMTA3 is claimed to negatively regulate transcription of EDS1. We show that EDS1 mRNA levels are no longer elevated in camta3 expressing DSC1-DN or DSC2-DN. Interestingly, we found that dsc1 and dsc2 null mutants do not suppress camta3, but camta3/dsc1/dsc2 triple mutants no longer exhibit autoimmunity. DSC1 and DSC2 were also shown to interact with CAMTA3 suggesting close guard-guardee relationships. This indicates that the increased levels of immune-related transcripts in camta3 are due to NLR activation and not to the loss of CAMTA3 as a transcriptional repressor of immunity.

Abstract Number: P17-565
Session Type: Poster