Novel Genes of Fusarium graminearum That Negatively Regulate Deoxynivalenol Production and Virulence

被引:88
作者
Gardiner, Donald M. [1 ]
Kazan, Kemal [1 ]
Manners, John M. [1 ]
机构
[1] CSIRO Plant Ind, Queensland Biosci Precinct, St Lucia, Qld 4067, Australia
关键词
CROWN ROT DISEASE; GIBBERELLA-ZEAE; MYCOTOXIN DEOXYNIVALENOL; TRICHOTHECENE BIOSYNTHESIS; TRICHODIENE SYNTHASE; TOXIN BIOSYNTHESIS; WILD-TYPE; IN-VITRO; WHEAT; SPOROTRICHIOIDES;
D O I
10.1094/MPMI-22-12-1588
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Fusarium head blight of wheat, caused by Fusarium graminearum, is a serious disease resulting in both reduced yields and contamination of grain with trichothecene toxins, with severe consequences for mammalian health. Recently, we have identified several related amine compounds such as agmatine and putrescine that promote the production of high levels of trichothecene toxins, such as deoxynivalenol (DON), in culture by F. graminearum and F. sporotrichioides. Here, a global analysis of fungal gene expression using the Affymetrix Fusarium GeneChip during culture under DON-inducing conditions compared with noninducing conditions is reported. Agmatine differentially regulated a large number of fungal genes, including both known and previously uncharacterized putative secondary metabolite biosynthetic gene clusters. In silico prediction of binding sites for the transcriptional regulator (TRI6) controlling TRI gene expression and gene expression analysis in a TRI6 mutant of F. graminearum showed that three of the differentially regulated genes were under the control of TRI6. Gene knock-out mutations of two of these genes resulted in mutants with massively increased production of DON and increased aggressiveness toward wheat. Our results not only identify a novel mechanism of negative regulation of DON production and virulence in F. graminearum but also point out the potential of this pathogen to evolve with an ability to produce massively increased amounts of toxins and increased virulence.
引用
收藏
页码:1588 / 1600
页数:13
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