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Transcriptomic analysis of Paenarthrobacter nicotinovorans ATCC 49919 nicotine metabolism [2]

ABSTRACT: Paenarthrobacter nicotinovorans pAO1 is a nicotine degrading microorganism that shows promising applications in converting nicotine-containing waste into useful green chemicals. Its biotechnological applications are nevertheless hampered by the lack of knowledge and tools to perform genetic and metabolic engineering. The objective of the work is to provide the first transcriptome of the strain and is a second step in our envisioned complete omics characterization of nicotine metabolism in P. nicotinovorans ATCC 49919. Acknowledgements. This work was supported by a grant of the Romanian Ministry of Education and Research, CNCS - UEFISCDI, project number PN-III-P4-ID-PCE-2020-0656, within PNCDI III.

ORGANISM(S): Paenarthrobacter nicotinovorans

PROVIDER: GSE279035 | GEO | 2024/11/26

REPOSITORIES: GEO

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Transcriptomic analysis of Paenarthrobacter nicotinovorans ATCC 49919 nicotine metabolism

Project description:Paenarthrobacter nicotinovorans pAO1 is a nicotine degrading microorganism that shows promising applications in converting nicotine-containing waste into useful green chemicals. Its biotechnological applications are nevertheless hampered by the lack of knowledge and tools to perform genetic and metabolic engineering. The objective of the work is to provide the first transcriptome of the strain and is a second step in our envisioned complete omics characterization of nicotine metabolism in P. nicotinovorans ATCC 49919. Acknowledgements. This work was supported by a grant of the Romanian Ministry of Education and Research, CNCS - UEFISCDI, project number PN-III-P4-ID-PCE-2020-0656, within PNCDI III.

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Project description:Perinatal smoke/nicotine exposure alters lung development and causes asthma in exposed offspring, transmitted transgenerationally. The mechanism underlying the transgenerational inheritance of perinatal smoke/nicotine-induced asthma remains unknown, but germline epigenetic modulations may play a role. Using a well-established rat model of perinatal nicotine-induced asthma, we determined the DNA methylation pattern of spermatozoa of F1 rats exposed perinatally to nicotine in F0 gestation. To identify differentially methylated regions (DMRs), reduced representation bisulfite sequencing was performed on spermatozoa of F1 litters. The top regulated gene body and promoter DMRs were tested for lung gene expression levels, and key proteins involved in lung development and repair were determined. The overall CpG methylation in F1 sperms across gene bodies, promoters, 5’UTRs, exons, introns, and 3’UTRs was not affected by nicotine exposure. However, the methylation levels were different between the different genomic regions. 81 CpG sites, 16 gene bodies, and 3 promoter regions were differentially methylated. Gene enrichment analysis of DMRs revealed pathways involved in oxidative stress, nicotine response, alveolar and brain development, and cellular signaling. Among the DMRs, Dio1 and Nmu were the most hypermethylated and hypomethylated genes, respectively. Gene expression analysis showed that the mRNA expression and DNA methylation were incongruous. Key proteins involved in lung development and repair were significantly different (FDR < 0.05) between the nicotine and placebo-treated groups. Our data show that DNA methylation is remodeled in offspring spermatozoa upon perinatal nicotine exposure. These epigenetic alterations may play a role in transgenerational inheritance of perinatal smoke/nicotine induced asthma.

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