Proctor Robert H, Plattner Ronald D, Desjardins Anne E, Busman Mark, Butchko Robert A E
National Center for Agricultural Utilization Research, Agricultural Research Service, U.S. Department of Agriculture, 1815 North University Street, Peoria, Illinois 61604, USA.
J Agric Food Chem. 2006 Mar 22;54(6):2424-30. doi: 10.1021/jf0527706.
Fumonisins are polyketide-derived mycotoxins produced by the maize pathogen Fusarium verticillioides. Previous analyses identified naturally occurring variants of the fungus that are deficient in fumonisin C-10 hydroxylation or that do not produce any fumonisins. In the current study, gene deletion and genetic complementation analyses localized the C-10 hydroxylation deficiency to a cytochrome P450 monooxygenase gene in the fumonisin biosynthetic gene (FUM) cluster. Sequence analysis indicated that the hydroxylation deficiency resulted from a single nucleotide insertion that caused a frame shift in the coding region of the gene. Genetic complementation localized the fumonisin-nonproduction phenotype to the polyketide synthase gene in the FUM cluster, and sequence analysis indicated that the nonproduction phenotype resulted from a nucleotide substitution, which introduced a premature stop codon in the coding region. These results provide the first direct evidence that altered fumonisin production phenotypes of naturally occurring F. verticillioides variants can result from single point mutations in the FUM cluster.
伏马毒素是由玉米病原菌轮枝镰孢菌产生的聚酮类衍生霉菌毒素。先前的分析鉴定出了该真菌的天然变体,这些变体缺乏伏马毒素C-10羟基化能力或不产生任何伏马毒素。在当前研究中,基因缺失和基因互补分析将C-10羟基化缺陷定位到伏马毒素生物合成基因(FUM)簇中的一个细胞色素P450单加氧酶基因。序列分析表明,羟基化缺陷是由单个核苷酸插入导致基因编码区发生移码引起的。基因互补将不产生伏马毒素的表型定位到FUM簇中的聚酮合酶基因,序列分析表明,不产生伏马毒素的表型是由一个核苷酸替换导致的,该替换在编码区引入了一个提前终止密码子。这些结果提供了首个直接证据,即天然存在的轮枝镰孢菌变体中伏马毒素产生表型的改变可能是由FUM簇中的单点突变引起的。