Bluhm B H, Kim H, Butchko R A E, Woloshuk C P
Crop Production & Pest Control Research Unit, USDA-ARS, West Lafayette, IN 47907, USA.
Mol Plant Pathol. 2008 Mar;9(2):203-11. doi: 10.1111/j.1364-3703.2007.00458.x.
Fumonisins comprise a class of carcinogenic mycotoxins produced by Fusarium verticillioides during colonization of maize kernels. In previous work, we identified ZFR1, which is predicted to encode a Zn(II)2Cys6 zinc finger transcription factor required for fumonisin B(1) (FB(1)) production during growth on kernels. In this study, we characterized the role of ZFR1 in colonizing maize kernels and inducing FB(1) biosynthesis. The ZFR1 deletion strain (Deltazfr1) grew approximately 2.5-fold less than the wild-type on endosperm tissue and a variety of other carbon sources, including glucose and amylopectin. However, the Deltazfr1 strain displayed higher alpha-amylase activity and expression of genes involved in starch saccharification than the wild-type, thus indicating that the reduced growth of the Deltazfr1 strain was not due to inhibition of amylolytic enzymes. In the wild-type strain, expression of six genes encoding putative sugar transporters was significantly greater on endosperm tissue than on germ tissue, and expression of at least three of the six genes was negatively affected by disruption of ZFR1. Intriguingly, disruption of FST1 had no effect on growth, kernel colonization or kernel pH but decreased FB(1) production by approximately 82% on maize kernels. Based on these findings, we hypothesize that ZFR1 controls FB(1) biosynthesis by regulating genes involved in the perception or uptake of carbohydrates.
伏马毒素是在玉米籽粒被轮枝镰孢菌侵染期间产生的一类致癌霉菌毒素。在之前的研究中,我们鉴定出了ZFR1,它被预测编码一种Zn(II)2Cys6锌指转录因子,该因子在籽粒上生长期间是伏马毒素B(1)(FB(1))产生所必需的。在本研究中,我们对ZFR1在侵染玉米籽粒和诱导FB(1)生物合成中的作用进行了表征。ZFR1缺失菌株(Δzfr1)在胚乳组织以及包括葡萄糖和支链淀粉在内的多种其他碳源上的生长速度比野生型慢约2.5倍。然而,Δzfr1菌株显示出比野生型更高的α-淀粉酶活性以及参与淀粉糖化的基因表达,因此表明Δzfr1菌株生长减缓并非由于淀粉酶的抑制。在野生型菌株中,六个编码假定糖转运蛋白的基因在胚乳组织上的表达明显高于在胚组织上的表达,并且这六个基因中至少有三个基因的表达受到ZFR1破坏的负面影响。有趣的是,FST1的破坏对生长、籽粒侵染或籽粒pH没有影响,但使玉米籽粒上的FB(1)产量降低了约82%。基于这些发现,我们推测ZFR1通过调节参与碳水化合物感知或摄取的基因来控制FB(1)的生物合成。