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

Date Published: May 22, 2019

Publisher: Public Library of Science

Author(s): Noor A. Abdelsamad, Gustavo C. MacIntosh, Leonor F. S. Leandro, Binod Bihari Sahu.

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

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.

Partial Text

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. In the last two decades, SDS was ranked among the top ten most damaging soybean diseases in the United States, with average yield losses ranging from 0.3 to 2 million metric tons per year [2, 3]. As a soilborne pathogen, Fv infect roots at early soybean growth stages, causing root rot and reduction in root biomass. The fungus then 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].

In this work, we investigated the effect of ethylene suppression and induction on soybean resistance against Fv infection. Previous studies have shown the importance of phytohormone signaling in resistance against plant diseases [31, 32], but to our knowledge, this is the first report directly testing the role of the ethylene hormone in the soybean-Fv interaction.

The results of this study support our hypothesis that the ethylene-signaling pathway is important in resistance against SDS. We observed a correlation between ethylene signaling, accumulation of defense-related genes, and SDS resistance in response to ethephon treatment. A limitation of our study is that ethephon was applied to soybean seedlings at VC stage, before Fv infection, and under controlled environmental conditions. Future work should validate the effect of ethephon on SDS under field conditions and at different application times. If ethylene is shown to enhance resistance against Fv infection in field conditions, then transcriptomic analysis of soybean seedlings in response to ethephon treatment is needed to identify resistant genes that could be incorporated into breeding against Fv.

 

Source:

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

 

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