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. 2023 Mar 15;13:4283. doi: 10.1038/s41598-023-31285-5

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© The Author(s) 2023

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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DAC treatment of mice infected with E. coli induces CpG demethylation at unique genomic loci and with greater strength in neonates versus juveniles. (A, B) Density plot of changes in CpG methylation frequency (Δβ) in (A) neonatal mice and (B) juvenile mice. DAC treatment more strongly induces demethylation (Δβ < 0) in neonates than in juveniles, which are less likely to be demethylated (Δβ > 0). (C) Venn diagram showing the number and overlap of differentially methylated genes with at least one differentially methylated CpG in DAC vs. DMSO across neonates and juveniles. (D–F) Over-representation analysis (ORA) from gProfiler showing GO: Biological Processes (GO:BPs) associated with genes differentially methylated in response to DAC treatment in (D) neonates, (E) juveniles, and (F) both.