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Transcriptomic and chromatin accessibility analyses of porcine alveolar macrophages exposed to Fumonisin B1

ABSTRACT: Fumonisin B1 (FB1) is a mycotoxin that poses a great threat to agricultural production and human and animal health. However, the molecular mechanism underlying the cytotoxic effect of FB1 to mammals has not been systematically elucidated. Here, we utilized the porcine alveolar macrophage cell line 3D4/21 as model, and applied RNA sequencing (RNA-seq) to analyze the genome-wide transcriptional alterations of mRNA, lncRNA, circRNA and miRNA before and after exposure to FB1 in six samples. To further reveal the underlying regulatory mechanism, we applied Assay for Transposase-Accessible Chromatin with high-throughput sequencing (ATAC-seq) to determine the genome-wide chromatin accessibility alterations in response to FB1-induced cytotoxicity. We anticipate that this dataset will serve as valuable resource for clarifying the transcriptional and regulatory mechanism underlying the cytotoxic effect of FB1, and facilitate the identification of the key genes and signaling pathways contributing to cellular response to FB1 exposure.

ORGANISM(S): Sus scrofa

PROVIDER: GSE190291 | GEO | 2022/11/09

REPOSITORIES: GEO

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Project description:PCD is a highly organised process that is involved in development and in an organisms response to biotic stresses (toxins and avirulent pathogens) and abiotic stresses (such as temperature, water availability, etc.). It is a genetically regulated form of cellular suicide, however in plants the underlying process is poorly understood. Although PCD may occur in response to different stimuli; we believe once it is triggered, one core mechanism is responsible for the cellular demise. It is our aim to identify the elements of this mechanism. We will do this by expanding on the work of a previous user of GARNet's GeneChip microarray facility, Dr. Jodi Swidzinski. She utilised an Arabidopsis cell suspension system; performing microarray analysis on both senescing, and heat shock induced PCD samples. This resulted in data showing that a large number of genes were upregulated (or downregulated) in response to both treatments. We are working under the premise that some of the genes that were similarly regulated under both treatments must be core PCD genes. However because of the large amount of data generated it is difficult to choose appropriate candidate genes (with any degree of confidence that they are core genes) for further study. We propose to use a third PCD-inducing treatment, involving a mycotoxin, to generate another population of microarray results. The mycotoxin we intend to use is Fumonisin B1 (FB1). This is an extremely potent compound that induces PCD by disrupting ceramide synthesis. We have found Arabidopsis protoplasts to be much more sensitive than cells to the toxin at low concentrations. Protoplasts are treated with 20mM FB1 and RNA is extracted at time points when 0%, 20% and 40% of protoplasts have died. This RNA is then pooled. RNA from methanol treated protoplasts is used as a control. We intend for these RNA samples to be subjected to GeneChip microarray analysis. This would identify genes differentially regulated due to FB1 treatment, which would be interesting in itself. However, by combining this data with that from previous work by Swidzinski (2002) we will be able to decrease the pool of possible core genes further, and increase the chances of selecting an appropriate candidate gene. This will both improve upon existing work and add value to an existing GARNet data set.

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Transcriptomic and chromatin accessibility analyses of porcine alveolar macrophages exposed to Fumonisin B1

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