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鉴定和功能表征负责 Fusaproliferin 生物合成的基因簇。

Identification and Functional Characterization of the Gene Cluster Responsible for Fusaproliferin Biosynthesis in .

机构信息

Institute of Bioanalytics and Agro-Metabolomics, Department of Agrobiotechnology (IFA-Tulln), University of Natural Resources and Life Sciences, Vienna (BOKU), Konrad-Lorenz-Str. 20, 3430 Tulln, Austria.

Institute of Microbial Genetics, Department of Applied Genetics and Cell Biology, University of Natural Resources and Life Sciences, Vienna (BOKU), Konrad-Lorenz-Str. 24, 3430 Tulln, Austria.

出版信息

Toxins (Basel). 2021 Jul 6;13(7):468. doi: 10.3390/toxins13070468.

DOI:10.3390/toxins13070468
PMID:34357940
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8310001/
Abstract

The emerging mycotoxin fusaproliferin is produced by and other related species. Several fungi from other taxonomic groups were also reported to produce fusaproliferin or the deacetylated derivative, known as siccanol or terpestacin. Here, we describe the identification and functional characterization of the genes encoding the fusaproliferin biosynthetic enzymes: a terpenoid synthase, two cytochrome P450s, a FAD-oxidase and an acetyltransferase. With the exception of one gene encoding a CYP450 (, FPRN_05484), knock-out mutants of the candidate genes could be generated, and the production of fusaproliferin and intermediates was tested by LC-MS/MS. Inactivation of the (FPRN_05485) terpenoid synthase gene led to complete loss of fusaproliferin production. Disruption of a putative FAD-oxidase (, FPRN_05486) did not only affect oxidation of preterpestacin III to terpestacin, but also of new side products (11-oxo-preterpstacin and terpestacin aldehyde). In the knock-out strains lacking the predicted acetyltransferase (, FPRN_05487) fusaproliferin was no longer formed, but terpestacin was found at elevated levels. A model for the biosynthesis of fusaproliferin and of novel derivatives found in mutants is presented.

摘要

真菌 Fusarium 属及其他相关种属产生的新型真菌毒素 Fusaproliferin。还有其他分类群的几种真菌也被报道能产生 Fusaproliferin 或去乙酰化衍生物，称为 Siccanol 或 Terpestacin。在此，我们描述了编码 Fusaproliferin 生物合成酶的基因的鉴定和功能特征：一种萜烯合酶、两种细胞色素 P450s、一种 FAD-氧化酶和一种乙酰基转移酶。除了编码一个细胞色素 P450（FPRN_05484）的一个基因外，候选基因的敲除突变体可以被生成，并通过 LC-MS/MS 测试 Fusaproliferin 和中间产物的产生。萜烯合酶基因（FPRN_05485）的失活导致 Fusaproliferin 的完全丧失。假定 FAD-氧化酶（FPRN_05486）的缺失不仅影响了 Preterpestacin III 向 Terpestacin 的氧化，还影响了新的侧产物（11-氧-Preterpstacin 和 Terpestacin 醛）的形成。在缺乏预测的乙酰基转移酶（FPRN_05487）的敲除菌株中，不再形成 Fusaproliferin，但发现 Terpestacin 水平升高。提出了 Fusaproliferin 及其在突变体中发现的新型衍生物生物合成的模型。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da42/8310001/3aa82660d1ed/toxins-13-00468-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da42/8310001/9a0a1e44657a/toxins-13-00468-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da42/8310001/8c18da5d4a26/toxins-13-00468-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da42/8310001/ede6a8622634/toxins-13-00468-g003a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da42/8310001/3aa82660d1ed/toxins-13-00468-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da42/8310001/9a0a1e44657a/toxins-13-00468-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da42/8310001/8c18da5d4a26/toxins-13-00468-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da42/8310001/ede6a8622634/toxins-13-00468-g003a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da42/8310001/3aa82660d1ed/toxins-13-00468-g004.jpg

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