Skip to main content
ARS Home » Research » Publications at this Location » Publication #188962


item Butchko, Robert
item Plattner, Ronald
item Proctor, Robert

Submitted to: Journal of Agricultural and Food Chemistry
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 10/13/2006
Publication Date: 11/16/2006
Citation: Butchko, R.A., Plattner, R.D., Proctor, R. 2006. Deletion analysis of FUM genes involved in tricarballylic ester formation during fumonisin biosynthesis. Journal of Agricultural Food & Chemistry. 54:9398-9404.

Interpretive Summary: Fumonisins are chemical compounds produced by the corn fungus Fusarium verticillioides which are harmful to both man and animals. F. verticillioides can cause ear and stalk rot on maize and can contaminate the corn kernels with fumonisins. In an effort to try to reduce or eliminate fumonisin contamination of corn, we are interested in understanding the genetics and biochemistry involved in the production of fumonisins. There are as many as 15 genes suspected to be involved in the production of fumonisins. One way in which to understand the function of a given gene is to disable that gene. Previously, this gene disabling technique, often referred to as a gene knockout, has been used to positively identify the role of many of the genes in the production of fumonisins. In this report, we have knocked out five of the genes suspected to be involved in fumonisin production. By studying the effects of knocking out each of these genes, we have been able to positively define the roles of four of these genes. They are all involved in forming a portion of the fumonisin molecule. These results allow us to better understand the biochemistry involved in fumonisin production and the genetic basis of fumonisin production. We hope to be able to use this information to devise novel methods for reducing or eliminating fumonisin contamination of corn.

Technical Abstract: Fumonisins are carcinogenic mycotoxins produced by the maize ear rot pathogen Gibberella moniliformis. These toxins consist of a linear polyketide-derived backbone substituted at various positions with an amine, one to four hydroxyl, two methyl and two tricarballylic (TCA) ester functions. In this study, we generated deletion mutants of G. moniliformis for five genes, FUM7, FUM10, FUMll, FUM14 and FUM16, in the fumonisin biosynthetic gene cluster. Deletions in four genes, predicted to encode unrelated proteins, all affected the TCA esters. FUM7 deletion mutants produced previously undescribed homologues of FB3 and FB4 with alkene functions in the TCA esters; FUM10 and FUM14 deletion mutants produced FB3 and FB4 homologues that lacked TCA functions; and FUM11 deletion mutants produced fumonisins that lacked one of the two TCA functions. These phenotypes indicate specific roles for FUM7, FUM10, FUM11 and FUM14 in fumonisin biosynthesis that are consistent with the predicted proteins encoded by each gene. Deletion of FUM16 had no effect on fumonisin production. The phenotypes of the deletion mutants provide further insight into fumonisin biosynthesis.