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. 2020 Sep 15;10:15086. doi: 10.1038/s41598-020-72155-8

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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 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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A hypothetical model for the functional interference of PARP1 with MyoD-dependent transcription. In undifferentiated cells the absence of MyoD activity at the regulatory regions of its targets prevents the induction of muscle genes, concomitantly with the presence of high levels of PARP1. Upon differentiation, the reduction of PARP1 levels and its decreased association with the regulatory regions increases the binding of MyoD and the induction of gene expression, accompanied by the accumulation of H3K4me3. When PARP1 is depleted, the binding of MyoD and the accumulation of H3K4me3 to the regulatory regions are further facilitated, resulting in increased up-regulation of MyoD targets.