Beyond toxicity: a regulatory role for mitochondrial cyanide

Abstract

In non-cyanogenic plants, cyanide is a co-product of ethylene and camalexin biosynthesis. To maintain cyanide at non-toxic levels, Arabidopsis plants express the mitochondrial β-cyanoalanine synthase CYS-C1. CYS-C1 knockout leads to an increased level of cyanide in the roots and leaves and a severe defect in root hair morphogenesis, suggesting that cyanide acts as a signaling factor in root development. During compatible and incompatible plant-bacteria interactions, cyanide accumulation and CYS-C1 gene expression are negatively correlated. Moreover, CYS-C1 mutation increases both plant tolerance to biotrophic pathogens and their susceptibility to necrotrophic fungi, indicating that cyanide could stimulate the salicylic acid-dependent signaling pathway of the plant immune system. We hypothesize that CYS-C1 is essential for maintaining non-toxic concentrations of cyanide in the mitochondria to facilitate cyanide's role in signaling.

Keywords: cell signaling; cyanide; mitochondria; plant immune response; root hair; β-cyanoalanine synthase.

Figure 1. Cyanide and the plant immune response. Pathogen attack induces the biosynthesis of hormones, mainly jasmonic acid (JA) and ethylene (ET) in response to necrotrophic pathogens and salicylic acid (SA) in response to biotrophic pathogens, although biotrophes can also induce ET biosynthesis. In our model, cyanide, which is produced concomitantly to ethylene, enters mitochondria where it generates a direct and/or indirect a signal that stimulates the SA-dependent response pathway.