Abstract

The Fusarium mycotoxin deoxynivalenol (DON) can cause cell death in wheat (Triticum aestivum), but can also reduce the level of cell death caused by heat shock in Arabidopsis (Arabidopsis thaliana) cell cultures. We show that 10 μg mL−1 DON does not cause cell death in Arabidopsis cell cultures, and its ability to retard heat-induced cell death is light dependent. Under dark conditions, it actually promoted heat-induced cell death. Wheat cultivars differ in their ability to resist this toxin, and we investigated if the ability of wheat to mount defense responses was light dependent. We found no evidence that light affected the transcription of defense genes in DON-treated roots of seedlings of two wheat cultivars, namely cultivar CM82036 that is resistant to DON-induced bleaching of spikelet tissue and cultivar Remus that is not. However, DON treatment of roots led to genotype-dependent and light-enhanced defense transcript accumulation in coleoptiles. Wheat transcripts encoding a phenylalanine ammonia lyase (PAL) gene (previously associated with Fusarium resistance), non-expressor of pathogenesis-related genes-1 (NPR1) and a class III plant peroxidase (POX) were DON-upregulated in coleoptiles of wheat cultivar CM82036 but not of cultivar Remus, and DON-upregulation of these transcripts in cultivar CM82036 was light enhanced. Light and genotype-dependent differences in the DON/DON derivative content of coleoptiles were also observed. These results, coupled with previous findings regarding the effect of DON on plants, show that light either directly or indirectly influences the plant defense responses to DON.

Highlights

  • Fusarium graminearum Schwabe [teleomorph Gibberella zeae (Schweinitz) Petch] andF. culmorum

  • We show the ability of DON and DON-producing F. graminearum to retard cell death caused by heat shock in Arabidopsis cell cultures is light dependent, and that DON enhanced heat-induced cell death in dark-grown cells

  • We used heat as an abiotic cell death inducer and determined whether light was necessary for DON-mediated inhibition of heat-induced cell death

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Summary

Introduction

F. culmorum (W.G. Smith) Saccardo cause diseases on the roots, stems and heads of cereal plants [1]. F. graminearum and F. culmorum commonly produce the trichothecene mycotoxin deoxynivalenol (DON) in infected plant tissue and this toxin acts as an aggressiveness factor for the pathogen during the development of root rot and FHB disease [2,3]. DON inhibits protein synthesis and its effect on wheat (Triticum aestivum L.) head tissue is similar to that of FHB disease, in that it bleaches the tissue [4,5]. Wheat genotypes differ in their response to DON; resistance to DON-induced bleaching is associated with resistance to the spread of FHB disease (type II resistance to FHB), but not with resistance to Fusarium infection (type I resistance to FHB) [4]

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