The cyanogenic syndrome in rubber tree Hevea brasiliensis: tissue-damage-dependent activation of linamarase and hydroxynitrile lyase accelerates hydrogen cyanide release

Abstract

Background and AimsThe release of hydrogen cyanide (HCN) from injured plant tissue affects multiple ecological interactions. Plant-derived HCN can act as a defence against herbivores and also plays an important role in plant–pathogen interactions. Crucial for activity as a feeding deterrent is the amount of HCN generated per unit time, referred to as cyanogenic capacity (HCNc). Strong intraspecific variation in HCNc has been observed among cyanogenic plants. This variation, in addition to genotypic variability (e.g. in Trifolium repens), can result from modifications in the expression level of the enzymes involved in either cyanogenic precursor formation or HCN release (as seen in Sorghum bicolor and Phaseolus lunatus). Thus, a modification or modulation of HCNc in reaction to the environment can only be achieved from one to the next generation when under genetic control and within days or hours when transcriptional regulations are involved. In the present study, it is shown that in rubber tree (Hevea brasiliensis) HCNc is modulated by post-translational activity regulation of the key enzymes for cyanide release.MethodsLinamarase (LIN) and hydroxynitrile lyase (HNL) activity was determined by colorimetric assays utilizing dissociation of the substrates p-nitrophenyl-β-d-glucopyranoside and acetone cyanohydrin, respectively.Key ResultsIn rubber tree leaves, LIN and HNL show up to ten-fold increased activity in response to tissue damage. This enzyme activation occurs within seconds and results in accelerated HCN formation. It is restricted to the damaged leaf area and depends on the severity of tissue damage.ConclusionsLIN and HNL activation (in contrast to genetic and transcriptional regulations) allows an immediate, local and damage type-dependent modulation of the cyanogenic response. Accordingly, this post-translational activation plays a decisive role in the defence of H. brasiliensis against herbivores as well as pathogens and may allow more flexible reactions in response to these different antagonists.

The Hevea brasiliensis AP2/ERF superfamily: from ethylene signalling to latex harvesting and physiological disease response

“…First, the peroxidation of lutoidic membranes releases coagulation factors leading to reactive oxygen species-type of TPD (ROS-TPD) (Jacob et al, 1989b). Secondly, oxidative stress may lead to lipid peroxidation in the plasma membrane, release of linamarase and linamarin resulting to cyanide production (Kadow et al, 2012). In a worse condition, a bark necrosis can occur resulting finally brown bast-type of TPD (BB-TPD).…”

The β‐cyanoalanine synthase pathway: beyond cyanide detoxification

“…Hydrolysis of cyanogenic glycosides in response to herbivory/tissue damage (Seigler ; Kadow et al . ) or during decomposition of plant material in soil (Widmer & Abawi ) leads to the release of cyanide. Degradation of glucosinolates in the Brassicaceae family (Donkin et al .…”

“…While the majority of these species are angiosperms, nearly 300 species of ferns and at least 48 species of gymnosperms synthesize these compounds (Harper et al 1976). Hydrolysis of cyanogenic glycosides in response to herbivory/tissue damage (Seigler 1991;Kadow et al 2012) or during decomposition of plant material in soil (Widmer & Abawi 2002) leads to the release of cyanide. Degradation of glucosinolates in the Brassicaceae family (Donkin et al 1995) and in camalexin biosynthesis in Arabidopsis thaliana (Böttcher et al 2009) can also generate cyanide.…”

Grazing intensity contributes to cyanogenic toxicity in savannah grasses in Baringo county

“…Several studies have detected a correlation between bitterness and HCNp (Lee et al 2013, p7755), as recognized in the common names of highly cyanogenic varieties of Prunus, such as bitter and sweet cherries (P. emarginata and P. avium, respectively) and almonds (P. amygdalus syn .P.dulcius). The level of plant defense chemicals is further influenced by damage (Kadow et al 2012. Several specialist herbivores not only tolerate CNglcs but also actually sequester them for use in their own arsenal of defense compounds against predators (Nishida 2002 In further support of these, Gleadow & Møller (2014) documented evidence that demonstrates that factors affecting CNglc concentration can be explained in terms of a resource-based trade-off between plant growth and defense.…”