期刊
MOLECULAR PLANT PATHOLOGY
卷 16, 期 9, 页码 987-999出版社
WILEY-BLACKWELL
DOI: 10.1111/mpp.12254
关键词
ammonium suppression; DON production; Gibberella zeae; nitrogen metabolism; TRI6 expression
资金
- National Major Project of Breeding for New Transgenic Organisms [2012ZX08009003]
- Nature Science Foundation of China [31271989]
- Program for New Century Excellent Talents in University
Deoxynivalenol (DON), a trichothecene mycotoxin produced by Fusarium graminearum, is harmful to humans and animals. Because different nitrogen sources are known to have opposite effects on DON production, in this study, we characterized the regulatory mechanisms of the AREA transcription factor in trichothecene biosynthesis. The areA mutant showed significantly reduced vegetative growth and DON production in cultures inoculated with hyphae. Suppression of TRI gene expression and DON production by ammonium were diminished in the areA mutant. The deletion of AREA also affected the stimulatory effects of arginine on DON biosynthesis. The AreA-green fluorescent protein (GFP) fusion complemented the areA mutant, and its localization to the nucleus was enhanced under nitrogen starvation conditions. Site-directed mutagenesis showed that the conserved predicted protein kinase A (PKA) phosphorylation site S874 was important for AreA function, indicating that AreA may be a downstream target of the cyclic adenosine monophosphate (cAMP)-PKA pathway, which is known to regulate DON production. We also showed that AreA interacted with Tri10 in co-immunoprecipitation assays. The interaction of AreA with Tri10 is probably related to its role in the regulation of TRI gene expression. Interestingly, the areA mutant showed significantly reduced PKA activity and expression of all three predicted ammonium permease (MEP) genes, in particular MEP1, under low ammonium conditions. Taken together, our results show that AREA is involved in the regulation of DON production by ammonium suppression and the cAMP-PKA pathway. The AreA transcription factor may interact with Tri10 and control the expression and up-regulation of MEP genes.
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