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. 2020 May 4;3:208. doi: 10.1038/s42003-020-0935-z

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© The Author(s) 2020

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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 7 — Restraint stress information, received by the central nervous system (CNS) and/or other sensing tissues, promotes expression of upd3 in peripheral somatic tissues. In germ cells, accumulated humoral Upd3 activates the JAK/STAT pathway, which subsequently activates the p38-dATF-2 pathway. Phosphorylated dATF-2 may be released from the promotor regions of its target genes, resulting in decreased H3K9me2 levels. Epigenetic marks may be retained in mature sperm and inherited by offspring. After fertilization, histone marks may act as inheritable epigenetic memory and regulate gene expression. We observed that genes involved in the one-carbon metabolic pathway were upregulated in offspring from the paternal restraint stress-exposed fathers, while genes involved in the respiratory metabolic pathway were downregulated. We assume that paternal restraint stress-induced- and dATF-2-mediated upregulation of the one-carbon cycle induces downregulation of respiratory metabolism due to a trade-off relationship between these two metabolic processes.