Ca2+ is an important target of cinnamaldehyde (CA) in Phytophthora capsici―the novel role of CA in controlling plant pathogen revealed by Chen's Lab

The pepper phytophthora blight disease caused by Phytophthora capsici is one of the most devastating plant diseases in the world. The increasing resistance of P. capsici to the common-used fungicides, such as mefenoxam and pyrimorph, has been widely found in many vegetable production regions. Thus, new fungicides aiming at different targets need to be timely developed to overcome this resistance. The recent research from Chen’s Lab in IFQS has just revealed that cinnamaldehyde (CA) could be an novel “green” antifungal agent for controlling P. capsici efficiently.
Cinnamaldehyde (CA), a major constituent of cinnamon essential oils, has been widely used as food additives due to its antimicrobial activity. Chen’s Lab has found that CA can also inhibit the growth of P. capsici effectively. Then, according to the growth experiment coupled with flow cytometry detection, the positive correlation between CA-induced growth stunt of P. capsici and CA-induced rapid efflux of Ca2+ has been well established. In addition, the application of antagonist suggested that CA induced rapid Ca2+ efflux and growth inhibition of P. capsici through Michael addition. The important role of Ca2+ in regulating fungal growth has been widely accepted. This research not only identifies the novel target of CA in fungi, but also provides direct evidence for developing CA as a novel plant-derived fungicide in controlling plant pathogen.
The research has been published online in PLOS ONE on October 1, 2013, which can be accessed at

Abstract (of the published paper)
As a destructive fungus-like plant pathogen, the oomycete Phytophthora capsici is unable to synthesize its own ergosterol as the potential target of fungicide cinnamaldehyde (CA). In this study, CA exerted efficient inhibitory effects on both mycelial growth (EC50=0.75 mM) and zoospore germination (MIC=0.4 mM) of P. capsici. CA-induced immediate Ca2+ efflux from zoospores could be confirmed by the rapid decrease in intracellular Ca2+ content determined by using Fluo-3 AM and the increase in extracellular Ca2+ concentration determined by using ICP-AES (inductively coupled plasma atomic emission spectrometry). Blocking Ca2+ influx with ruthenium red and verapamilled to a higher level of CA-induced Ca2+ efflux, suggesting the simultaneous occurrence of Ca2+ influx along with the Ca2+ efflux under CA exposure. Further results showed that EGTA-induced decrease intracellular Ca2+ gave rise to the impaired vitality of P. capsici while the addition of exogenous Ca2+ could suppress the growth inhibitory effect of CA. These results suggested that Ca2+ efflux played an important role in CA-induced growth inhibition of P. capsici. The application of 3-phenyl-1-propanal, a CA analog without α,β- unsaturated bond, resulted in a marked Ca2+ influx in zoospores but did not show any growth inhibitory effects. In addition, exogenous cysteine, an antagonist against the Michael addition (the nucleophilic addition of a carbanion or another nucleophile) between CA and its targets, could attenuate CA-induced growth inhibition of P. capsici by suppressing Ca2+ efflux. Our results suggest that CA inhibits the growth of P. capsici by stimulating a transient Ca2+ efflux via Michael addition, which provides important new insights into the antimicrobial action of CA.

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