Autoimmunity in Arabidopsis acd11 Is Mediated by Epigenetic Regulation of an Immune Receptor

Abstract

Certain pathogens deliver effectors into plant cells to modify host protein targets and thereby suppress immunity. These target modifications can be detected by intracellular immune receptors, or Resistance (R) proteins, that trigger strong immune responses including localized host cell death. The accelerated cell death 11 (acd11) “lesion mimic” mutant of Arabidopsis thaliana exhibits autoimmune phenotypes such as constitutive defense responses and cell death without pathogen perception. ACD11 encodes a putative sphingosine transfer protein, but its precise role during these processes is unknown. In a screen for lazarus (laz) mutants that suppress acd11 death we identified two genes, LAZ2 and LAZ5. LAZ2 encodes the histone lysine methyltransferase SDG8, previously shown to epigenetically regulate flowering time via modification of histone 3 (H3). LAZ5 encodes an RPS4-like R-protein, defined by several dominant negative alleles. Microarray and chromatin immunoprecipitation analyses showed that LAZ2/SDG8 is required for LAZ5 expression and H3 lysine 36 trimethylation at LAZ5 chromatin to maintain a transcriptionally active state. We hypothesize that LAZ5 triggers cell death in the absence of ACD11, and that cell death in other lesion mimic mutants may also be caused by inappropriate activation of R genes. Moreover, SDG8 is required for basal and R protein-mediated pathogen resistance in Arabidopsis, revealing the importance of chromatin remodeling as a key process in plant innate immunity.

Retromer Contributes to Immunity-Associated Cell Death in Arabidopsis

“…Suppression appeared relatively weak compared with other laz mutants Palma et al, 2010), as cell death symptoms were visible in older leaf stages of laz4-1 acd11-1 nahG plants 5 d after BTH treatment ( Figure 1A). However, cell death was more strongly attenuated in newly emerging leaves, which allowed laz4-1 acd11-1 nahG plants to survive throughout development to flower and set seed, in marked contrast with acd11-1 nahG plants (Supplemental Figure 1).…”

“…Mutants expressing autoimmunity-and PCD-related phenotypes are good genetic models to identify components of defense and cell death pathways (Moeder and Yoshioka, 2008;Palma et al, 2010;Bonardi et al, 2011). One of these is the recessive accelerated cell death11 (acd11) Arabidopsis mutant, which exhibits constitutive activation of immune responses and PCD due to disruption of a ceramide-1-phosphate transfer protein (Brodersen et al, 2002(Brodersen et al, , 2005Simanshu et al, 2014).…”

“…In acd11 nahG, cell death is triggered upon application of the salicylic acid agonist benzothiadiazole-S-methyl ester (BTH). We previously used this to isolate acd11 suppressor mutants, termed lazarus (laz) Palma et al, 2010). These analyses showed that lethality in acd11 fully depends on the NB-LRR immune receptor LAZ5 and that LAZ2, a histone H3 lysine 36 methyltransferase, is required for LAZ5 expression (Palma et al, 2010).…”

“…We previously used this to isolate acd11 suppressor mutants, termed lazarus (laz) Palma et al, 2010). These analyses showed that lethality in acd11 fully depends on the NB-LRR immune receptor LAZ5 and that LAZ2, a histone H3 lysine 36 methyltransferase, is required for LAZ5 expression (Palma et al, 2010). This indicates that loss of ACD11 results in inappropriate LAZ5 activation in the absence of pathogen effector recognition.…”

Two linked pairs of Arabidopsis TNL resistance genes independently confer recognition of bacterial effector AvrRps4

“…TAO1 contributes to disease resistance against Pst DC3000 carrying AvrB in Arabidopsis 56 and LAZ5 is required for the lesion mimic mutant acd11 (ref. 57). At5g45050 and At5g45060 were hitherto uncharacterized.…”