Characterization of a Fusarium graminearum Salicylate Hydroxylase

Salicylic acid (SA) plays an important role in regulating plant defense responses against pathogens. However, pathogens have evolved ways to manipulate plant SA-mediated defense signaling. causes Fusarium head blight (FHB) and reduces crop yields and quality by producing various mycotoxins. In this...

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Veröffentlicht in:Frontiers in microbiology 2019-01, Vol.9, p.3219
Hauptverfasser: Hao, Guixia, Naumann, Todd A, Vaughan, Martha M, McCormick, Susan, Usgaard, Thomas, Kelly, Amy, Ward, Todd J
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Sprache:eng
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Zusammenfassung:Salicylic acid (SA) plays an important role in regulating plant defense responses against pathogens. However, pathogens have evolved ways to manipulate plant SA-mediated defense signaling. causes Fusarium head blight (FHB) and reduces crop yields and quality by producing various mycotoxins. In this study, we aimed to identify the salicylate hydroxylase in and determine its role in wheat head blight development. We initially identified a gene in strain NRRL 46422 that encodes a putative salicylate hydroxylase (designated ). However, the deletion mutant showed a similar ability to degrade SA as wild-type strain 46422; nor did overexpression of FgShyC in convert SA to catechol. The results indicate that is not involved in SA degradation. Further genome sequence analyses resulted in the identification of eight salicylate hydroxylase candidates. Upon addition of 1 mM SA, FGSG_03657 (designated ), was induced approximately 400-fold. Heterologous expression of FgShy1 in converted SA to catechol, confirming that FgShy1 is a salicylate hydroxylase. Deletion mutants of were greatly impaired but not completely blocked in SA degradation. Expression analyses of infected tissue showed that was induced during infection, but virulence assays revealed that deletion of FgShy1 alone was not sufficient to affect FHB severity. Although the deletion mutant did not reduce pathogenicity, we cannot rule out that additional salicylate hydroxylases are present in and characterization of these enzymes will be necessary to fully understand the role of SA-degradation in FHB pathogenesis.
ISSN:1664-302X
1664-302X
DOI:10.3389/fmicb.2018.03219