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Fusarium graminearum is able to detoxify cereal defense compounds (tryptamine-derived hydroxycinnamic acid amides) and to convert the released tryptamine into auxin G. ADAM (1), P. Spörhase (2), P. Fruhmann (3), E. Beltran Iturat (4), A. Bartholomäus (1), A. Stadler (1), C. Schmeitzl (1), G. Wiesenberger (1), B. Kluger (5), M. Doppler (6), C. Büschl (6), R. Krska (4), R. Schuhmacher (6), F. Berthiller (4) (1) Univ. of Natural Resources and Life Sciences, Vienna (BOKU), Dpt. of Applied Genetics and Cell Biol., Austria; (2) Univ. of Natural Resources and Life Sciences, Vienna (BOKU), Dpt. of Applied Genetics and Cell Biol., Austria; (3) TU Vienna, Inst. of Applied Synthetic Chemistry, Austria; (4) Univ. Nat. Res. and Life Sci. (BOKU), Dpt. IFA Tulln, Center for Analytical Chemistry, Austria; (5) bernhard.kluger@boku.ac.at, Austria; (6) Univ. Nat. Res. and Life Sci. (BOKU), Dpt. IFA Tulln, Center for Analytical Chemistry, Austria
The mycotoxin producing ascomycete Fusarium graminearum causes the agronomically important plant diseases Fusarium head blight of cereals and ear rot of maize. Transcriptome studies showed that infection with F. graminearum upregulates tryptophan biosynthesis genes and tryptophan decarboxylase in barley and other monocot hosts. The resulting tryptamine (TAM) is conjugated with various hydroxycinnamic acids to form coumaroyl-tryptamine, feruloyl-tryptamine, etc. We have synthesized TAM containing hydroxycinnamic acids (HCAAs) and tested their activity against F. graminearum. Germination of conidia was delayed in a dose dependent manner, but after a short lag phase growth was indistinguishable from control. caffeoyl-tryptamine at very high concentrations caused a dose dependent growth reduction. We found that F. graminearum secretes amidohydrolase activity which is able to inactivate HCAAs. Released TAM was converted into indole 3-acetic acid (IAA) in high yield. F. graminearum infection of susceptible wheat resulted in highly elevated levels of IAA, inactive IAA-glucoside and IAA-Asp, and oxidized IAA as determined by LC-MS/MS. We propose that F. graminearum is able to subvert plant defense by triggering auxin signaling, and that induction of TAM-containing HCAAs might even lead to susceptibility of infected plants. Host mechanisms leading to more efficient inactivation of auxin or to reduced auxin signaling might be relevant for Fusarium resistance breeding.
Abstract Number:
P16-439, C12-3 Session Type:
Poster
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