Abstract

Zearalenone (ZEA) is one of the main mycotoxins widely spread in contaminated cereal crops, which poses a great threat to food safety as well as human and animal health. Biological control strategies are emerging as important solutions to eliminate mycotoxin contaminations. However, molecular mechanisms underlying ZEA cytotoxic effects are only partly understood. Noncoding RNAs and chromatin accessibilities are important regulators of gene expression and implicate in a variety of biological processes. Here, we established a study model of porcine intestinal epithelial cells upon ZEA exposure and presented a RNA-seq dataset for mRNA, microRNA, and lncRNA profiling in 18 experimental samples. In addition, chromatin accessibilities of four samples were also explored by ATAC-seq. This dataset will shed new light on gene expression profiling and transcriptional regulation of animal cells in the response to ZEA exposure, which further contributes to detecting biomarkers and drug targets for predicting and controlling ZEA contamination.

Highlights

  • Zearalenone (ZEA) is one the main mycotoxins produced by a variety of Fusarium fungal species and widely spread in contaminated cereal crops including maize, wheat, barley and oats[1]

  • Biological control strategies are emerging as promising solutions to eliminate mycotoxin contaminations

  • Disruption of gene expression programs is an important event through which mycotoxins exert cytotoxic effects

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Summary

Background & Summary

Zearalenone (ZEA) is one the main mycotoxins produced by a variety of Fusarium fungal species and widely spread in contaminated cereal crops including maize, wheat, barley and oats[1]. Recent studies have preliminarily investigated the effects of ZEA exposure on genome wide gene expression in porcine epithelial cells[7,8]. The regulatory networks involved in gene expression alterations in animal cells upon ZEA exposure remain largely unknown. We performed genome-wide analyses of the expressions of mRNA, miRNA, and lncRNA in porcine intestinal epithelial cells upon ZEA exposure (Fig. 1a). These data will provide comprehensive insight into gene expression profiles and transcriptional regulation of animal cells in the response to ZEA exposure, which may aid the detection of biomarkers and drug targets for predicting and controlling ZEA contamination

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