Abstract
Fusicoccin is the α glucoside of a carbotricyclic diterpene, produced by the fungus Phomopsis amygdali (previously classified as Fusicoccum amygdali), the causal agent of almond and peach canker disease. A great interest in this molecule started when it was discovered that it brought about an irreversible stomata opening of higher plants, thereby inducing the wilting of their leaves. Since then, several studies were carried out to elucidate its biological activity, biosynthesis, structure, structure-activity relationships and mode of action. After sixty years of research and more than 1800 published articles, FC is still the most studied phytotoxin and one of the few whose mechanism of action has been elucidated in detail. The ability of FC to stimulate several fundamental plant processes depends on its ability to activate the plasma membrane H+-ATPase, induced by eliciting the association of 14-3-3 proteins, a class of regulatory molecules widespread in eukaryotes. This discovery renewed interest in FC and prompted more recent studies aimed to ascertain the ability of the toxin to influence the interaction between 14-3-3 proteins and their numerous client proteins in animals, involved in the regulation of basic cellular processes and in the etiology of different diseases, including cancer. This review covers the different aspects of FC research partially treated in different previous reviews, starting from its discovery in 1964, with the aim to outline the extraordinary pathway which led this very uncommon diterpenoid to evolve from a phytotoxin into a tool in plant physiology and eventually into a 14-3-3-targeted drug.
Highlights
In the memory of Alessandro Ballio, a man of science esteemed throughout the world
The history of FC began with studies regarding the canker disease induced by the fungus P. amygdali on almond and peach trees, which caused severe economic losses in the south of Italy in the 1960s
The discovery that phytotoxicity was due to the ability of FC to irreversibly open stomata in all higher plants, despite the fungus is a pathogen of a restricted number of plant species, fueled studies aimed to discover the general process underlying FC effects in plant cells, which resulted in the ability of the toxin to stimulate the H+ -ATPase of the plasma membrane, the master enzyme for the regulation of ion and nutrient transport in plants
Summary
The effect on distal leaves led to the hypothesis that systemic symptoms could be due to the translocation to non-infected tissues of one or more phytotoxins produced by the fungus during infection. This hypothesis prompted studies aimed to their isolation from culture filtrates of P. amygdali and their successive chemical and biological characterization [3]. The main diterpene-glucoside isolated, together with several related minor metabolites, was originally named FC A This compound was able to reproduce part of the disease symptoms, such as the wilting of leaves [2,4,5], due to its ability to induce irreversible stomata openings and consequent uncontrolled transpiration [5]. FC was isolated from green peaches artificially inoculated with P. amygdali and from almond shoots naturally infected by the fungus, definitely proving that FC is a vivotoxin [6]
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