Dose-dependent activator of the defense response against virulent pathogens, including bacteria, fungi and oomycetes, that acts in a positive feedback loop with the defense signal salicylic acid (SA) (PubMed:14507999, PubMed:20520716, PubMed:10488236, PubMed:16297071, PubMed:19144005). Regulates the salicylic acid (SA) signaling pathway leading to cell death and modulating cell fate (e.g. cell enlargement and/or cell division) (PubMed:14507999, PubMed:10488236, PubMed:11722764). In response to SA signaling, triggers the accumulation of FLS2 at the plasma membrane, thus priming defenses (PubMed:24923602). Involved in SA-dependent freezing signaling and tolerance (PubMed:19959255). Component of large complexes containing, at least, FLS2, HSP70 and ACD6 in endoplasmic reticulum, plasma membrane and soluble fraction. Associated with HSP70 proteins during endoplasmic reticulum-associated degradation (ERAD). Reduced complex levels upon benzothiazole (BTH) treatment. Constitutively undergoes endoplasmic reticulum-associated degradation (ERAD), via ubiquitination and subsequent degradation by the proteasome. During salicylic acid (SA) signaling, the soluble pool decreases, whereas the plasma membrane pool increases. Basal expression requires light and salicylic acid (SA). Expression in leaves increases with age. Accumulates in systemic uninfected tissues during Pseudomonas syringae infection or upon benzothiazole (BTH) treatment. Induced by light, but repressed by dark (PubMed:14507999). Accumulates upon MG132 treatment, a proteasome inhibitor. Target of endoplasmic reticulum-associated degradation (ERAD) when ubiquitinated (PubMed:24923602). Ubiquitinated. Reduced responsiveness to benzothiazole (BTH) and upon P. syringae infection with reduced salicylic acid (SA) levels and increased disease susceptibility and attenuated defenses (PubMed:14507999). Increased sensitivity to biotrophic fungi (e.g. Golovinomyces orontii T1 and G. cichoracearum UCSC1), biotrophic oomycetes (e.g. Hyaloperonospora arabidopsidis Noco2) and hemi-biotrophic bacteria (e.g. Pseudomonas syringae pv. tomato DC3000) (PubMed:20520716). Sequence variations impacting defense responses are observed between cultivars. Enhanced resistance is correlated with a substantial reduction in vegetative biomass. The dominant gain-of-function mutant acd6-1 and over-expressing plant ACD6-o is dwarf and shows spontaneous cell death and increased disease resistance, as well as increased defenses and better responsiveness to salicylic acid (SA). These symptoms are SA-dependent (PubMed:14507999, PubMed:20520716, PubMed:10488236, PubMed:16297071, PubMed:19144005). In acd6-1, constitutively high free and total SA levels leading to collapsed dead cells with adjacent enlarged cells in the palisade parenchyma cell layer. This phenotype is absent in NahG background, in which SA is degraded (PubMed:11722764). Strong accumulation of camalexin (an anti-fungal compound) and SA in acd6-1 (PubMed:19144005). The mutant acd6-1 exhibits freezing sensitivity, this sensitivity is suppressed in nahG background (PubMed:19959255).