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Molecules 2017, 22(10), 1799; doi:10.3390/molecules22101799

Equol, a Clinically Important Metabolite, Inhibits the Development and Pathogenicity of Magnaporthe oryzae, the Causal Agent of Rice Blast Disease

1
State Key Laboratory Breeding Base for Zhejiang Sustainable Pest and Disease Control, Institute of Plant Protection and Microbiology, Zhejiang Academy of Agricultural Sciences, Hangzhou 310021, China
2
The Key Laboratory for Quality Improvement of Agricultural Products of Zhejiang Province, School of Agricultural and Food Sciences, Zhejiang Agriculture and Forest University, Hangzhou 311300, China
*
Authors to whom correspondence should be addressed.
Received: 28 September 2017 / Revised: 16 October 2017 / Accepted: 18 October 2017 / Published: 24 October 2017
(This article belongs to the Collection Bioactive Compounds)
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Abstract

Equol, a metabolite of soybean isoflavone daidzein, has been proven to have various bioactivities related to human health, but little is known on its antifungal activity to plant fungal pathogens. Magnaporthe oryzae is a phytopathogenic fungus that causes rice blast, a devastating disease on rice. Here, we demonstrated that equol influences the development and pathogenicity of M. oryzae. Equol showed a significant inhibition to the mycelial growth, conidial generation and germination, and appressorial formation of M. oryzae. As a result, equol greatly reduced the virulence of M. oryzae on rice and barley leaves. The antifungal activity of equol was also found in several other plant fungal pathogens. These findings expand our knowledge on the bioactivities of equol. View Full-Text
Keywords: equol; antifungal activity; plant pathogen; fungal pathogenicity; Magnaporthe oryzae equol; antifungal activity; plant pathogen; fungal pathogenicity; Magnaporthe oryzae
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Wang, J.; Li, L.; Yin, Y.; Gu, Z.; Chai, R.; Wang, Y.; Sun, G. Equol, a Clinically Important Metabolite, Inhibits the Development and Pathogenicity of Magnaporthe oryzae, the Causal Agent of Rice Blast Disease. Molecules 2017, 22, 1799.

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