Deletion Analysis of FUM Genes Involved in Tricarballylic Ester Formation during Fumonisin Biosynthesis
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- 作者：Robert A. E. Butchko ; Ronald D. Plattner ; Robert H. Proctor
- 刊名：Journal of Agricultural and Food Chemistry
- 出版年：2006
- 出版时间：December 13, 2006
- 年：2006
- 卷：54
- 期：25
- 页码：9398 - 9404
- 全文大小：130K
- 年卷期：v.54,no.25(December 13, 2006)
- ISSN：1520-5118
文摘
Fumonisins are carcinogenic mycotoxins produced by the maize ear rot pathogen Gibberellamoniliformis (anamorph Fusarium verticillioides). These toxins consist of a linear polyketide-derivedbackbone substituted at various positions with an amine, one to four hydroxyl, two methyl, and twotricarballylic ester functions. In this study, we generated and characterized deletion mutants of G.moniliformis for five genes, FUM7, FUM10, FUM11, FUM14, and FUM16 in the fumonisin biosyntheticgene cluster. Functional analysis of mutants in four genes, predicted to encode unrelated proteins,affected formation of the tricarballylic esters. FUM7 deletion mutants produced a previouslyundescribed homologue of fumonisin B1 with an alkene function in both tricarballylic esters, FUM10and FUM14 deletion mutants produced homologues of fumonisin B3 and fumonisin B4 that lacktricarballylic ester functions, and FUM11 deletion mutants produced fumonisins that lack one of thetricarballylic ester functions. These phenotypes indicated specific roles for FUM7, FUM10, FUM11,and FUM14 in fumonisin biosynthesis that are consistent with the predicted proteins encoded byeach gene. Deletion of FUM16 had no apparent effect on fumonisin production. The phenotypes ofthe deletion mutants provide further insight into the order of steps in fumonisin biosynthesis.