Induction of ethylene inhibits development of soybean sudden death syndrome by inducing defense-related genes and reducing Fusarium virguliforme growth.

Noor A Abdelsamad,Leonor F S Leandro,Gustavo C Macintosh

doi:10.1371/journal.pone.0215653

Noor A Abdelsamad, Leonor F S Leandro + Show 1 more

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https://doi.org/10.1371/journal.pone.0215653

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Abstract

Ethylene is a gaseous hormone that regulates plant responses to biotic and abiotic stresses. To investigate the importance of ethylene in soybean resistance to Fusarium virguliforme (Fv), the causal agent of sudden death syndrome (SDS), soybean cultivars Williams 82 (SDS-susceptible) and MN1606 (SDS-resistant) were treated 24 h before and 24h after Fv inoculation with either ethephon (ethylene inducer), cobalt chloride (ethylene biosynthesis inhibitor), or 1-MCP (ethylene perception inhibitor). Inoculated plants were grown for 21 days at 24°C in the greenhouse and then evaluated for SDS severity and expression of soybean defense genes. In both cultivars, plants treated with ethephon showed lower SDS foliar severity compared to the other treatments, whereas those treated with cobalt chloride or 1-MCP showed the same or higher SDS foliar severity compared to the water-treated control. Ethephon application resulted in activation of genes involved in ethylene biosynthesis, such as ethylene synthase (ACS) and ethylene oxidase (ACO), and genes involved in soybean defense response, such as pathogenesis-related protein (PR), basic peroxidase (IPER), chalcone synthase (CHS), and defense-associated transcription factors. Cobalt chloride and 1-MCP treatments had little or no effect on the expression of these genes. In addition, ethephon had a direct inhibitory effect on in-vitro growth of Fv on PDA media. Our results suggest that ethephon application inhibits SDS development directly by slowing Fv growth and/or by inducing soybean ethylene signaling and the expression of defense related genes.

Highlights

Sudden death syndrome (SDS), caused by the soilborne fungus Fusarium virguiforme (Fv) [1] is one of the most damaging diseases to soybean production in North and South America
21-day-old cultures on potato dextrose agar (PDA) were flooded with 20 ml of sterile distilled water (SDW), the conidia were dislodged with a rubber policeman, and the suspension was filtered through a double layer of sterile cheesecloth
Fusarium virguliforme infection triggers ethylene biosynthesis in soybean To examine whether Fv inoculation could induce ethylene biosynthesis in SDS resistance and susceptible soybean cultivars, the expression of key ethylene biosynthesis genes, 1-aminocyclopropane-1-carboxylic acid synthase (ACS), and 1-aminocyclopropane-1-carboxylic acid oxidase (ACO), were quantified in roots at 2 and 4 days post inoculation (DPI) and compared to time 0

Summary

Introduction

Sudden death syndrome (SDS), caused by the soilborne fungus Fusarium virguiforme (Fv) [1] is one of the most damaging diseases to soybean production in North and South America. Ethylene induction inhibits soybean sudden death syndrome the United States, with average yield losses ranging from 0.3 to 2 million metric tons per year [2, 3]. Fv infect roots at early soybean growth stages, causing root rot and reduction in root biomass. The fungus releases phytotoxins that cause foliar interveinal chlorosis and necrosis and premature defoliation; these foliar symptoms usually appear during reproductive growth stages [4, 5]. Cool (15 ̊C), wet soil early in the growing season, followed by intermediate temperatures (22–24 ̊C) during soybean reproductive development, are favorable environmental conditions for SDS symptom development [6]

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