Abstract
For thousands of years, fermentation products of the filamentous fungi Monascus spp. have been used extensively in the food and pharmaceutical industries. However, their development is limited because of the health threats from the mycotoxin citrinin, known to be produced by these fungi. Citrinin is recognized as a hepato-nephrotoxin which possesses potential genotoxicity, tumorigenicity, carcinogenicity, embryotoxicity, and teratogenicity. Studies have shown that citrinin biosynthesis is intimately related to pksCT, orf1, ctnA, orf3, ctnB and ctnG. The ctnE gene, which is located 3.3kb upstream of ctnA, encodes a protein that showed significant similarity to the dehydrogenase. In this study, the role of ctnE in citrinin biosynthesis was investigated by means of gene knockout technology. The ctnE disruptant significantly reduced citrinin production by 96%, which suggested that ctnE is important in citrinin biosynthesis. Moreover, the mutant produced 40% more pigments than the wild-type. This work contributes to the study of the citrinin biosynthesis pathway in Monascus, and the methodology described in this article can fundamentally lower the risk of citrinin contamination in Monascus aurantiacus Li AS3.4384 which has important significance for food safety.
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