A plant peroxisome lipase, SSD5, is required for steryl ester accumulation and activation of autoimmunity

Excess cellular sterol is harmful in mammals and plants, but the mechanisms why are awaiting clarification. Here we find a strong autoimmune response to be associated to excess endoplasmic reticulum (ER) sterols. This was obtained by studying a plant peroxisome lipase, SSD5, required for the lesion phenotype of the Arabidopsis syntaxin mutant, pen1 syp122 . SSD5 is a lipase with a catalytic triad including a GxSxG motif localized to a subdomain of the peroxisome periphery. Lipidomics revealed reduced steryl ester levels in pen1 syp122 when SSD5 is mutated. This involvement in sterol homeostasis was confirmed by a requirement of SSD5 for the lesions of hise1 psat1 that suffers from excess ER sterol. These data suggest SSD5 is contributing to a peroxisome-located segment of the sterol biosynthesis pathway. SSD5’s contribution to the pen1 syp122 autoimmunity is not associated with nine highly diverse down-stream immune components, and SSD5 does not influence general plant disease levels and immunity. Therefore, our data indicated SSD5 as well as ER sterol functions up-stream of immune activation. This in turn suggests plant excess ER sterol to activate one or more immune receptors.