4.5 Article

Carbon Sources Influence Fumonisin Production in Fusarium proliferatum

期刊

PROTEOMICS
卷 17, 期 19, 页码 -

出版社

WILEY
DOI: 10.1002/pmic.201700070

关键词

carbon source; fusarium proliferatum; fumonisin; proteome; reactive oxygen species

资金

  1. National Natural Science Foundation of China [31701657, 31401593, 31322044]
  2. China Postdoctoral Program for Innovative Talents [BX201600170]
  3. China Postdoctoral Science Foundation [2017M610559]
  4. National Key Research and Development Program of China [2016YFD0400904, 2016YFD0400902]
  5. Science and Technology Planning Project of Guangdong Province [2015B090901058]
  6. Science and Technology Planning Project of Guangzhou [201604020048]
  7. Science and Technology Service Network Initiative of Chinese Academy of Sciences [KFJ-EW-STS-118]
  8. Talent Program of Guangdong Province [2014TX01N049]

向作者/读者索取更多资源

Fusarium proliferatum is a worldwide fungal pathogen that produces fumonisins which are harmful to animal and human health. However, environmental factors affecting fumonisin biosynthesis in F. proliferatum are not well understood. Based on our preliminary results, in this study, we investigated the effect of sucrose or mannose as the sole carbon source on fumonisin B (FB) production by F. proliferatum and studied their underlying mechanisms via proteome and gene expression analysis. Our results showed that mannose, used as the sole carbon source, significantly blocked fumonisin B-1 and B-2 production by F. proliferatum as compared with the use of sucrose. Fifty-seven differentially expressed proteins were successfully identified. The downregulated proteins in the mannose-cultured strain were mainly involved in carbon metabolism, response to stress, and methionine metabolism, as compared with the sucrose-cultured strain. Moreover, quantitative real-time PCR analysis indicated that expression of several key genes involved in FB biosynthetic pathway and in transcription regulation were significantly downregulated in the mannose-cultured F. proliferatum, whereas expression of histone deacetylation-related genes were significantly upregulated. These results suggested that the blockage of FB biosynthesis by mannose was associated with the decreases in conversion of acetyl-CoA to polyketide, methionine biosynthesis, and NADPH regeneration. More importantly, milder oxidative stress, downregulated expression of genes involved in biosynthetic pathway and transcription regulation, and upregulated expression of genes with histone deacetylation possibly were responsible for the blockage of FB biosynthesis in F. proliferatum.

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