PMR4-dependent cell wall depositions are a consequence but not the cause of temperature-induced autoimmunity.

Plants possess a well-balanced immune system that is required for defense against pathogen infections. In autoimmune mutants or necrotic crosses, an intrinsic temperature-dependent imbalance leads to constitutive immune activation, resulting in severe damage or even death of plants. Recently, cell wall depositions were described as one of the symptoms following induction of the autoimmune phenotype in Arabidopsis saul1-1 mutants. However, the regulation and function of these depositions remained unclear. Here, we show that cell wall depositions, containing lignin and callose, were a common autoimmune feature and were deposited in proportion to the severity of the autoimmune phenotype at reduced ambient temperatures. When plants were exposed to reduced temperature for periods insufficient to induce an autoimmune phenotype, the cell wall depositions were not present. After low temperature intervals, sufficient to induce autoimmune responses, cell wall depositions correlated with a point of no return in saul1-1 autoimmunity. Although cell wall depositions were largely abolished in saul1-1 pmr4-1 double mutants lacking SAUL1 and the callose synthase gene GSL5/PMR4, their phenotype remained unchanged compared to that of the saul1-1 single mutant. Our data showed that cell wall depositions generally occur in autoimmunity, but appear not to be the cause of autoimmune phenotypes.

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