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. 2019 Jun 24;9:9195. doi: 10.1038/s41598-019-45477-5

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© The Author(s) 2019

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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PAX1 regulates phosphatases’ expression by recruiting the histone methyltransferase SET1B. The status of histone H3K4 and H3K9 trimethylation within the PTPRR promoter in PAX1-expressing cells after EGF treatment. (A) HeLa- and (B) SiHa-PAX1-expressing cells. (C,D) Promoter methylation status of phosphatase genes, in PAX1-expressing cells, after EGF treatment. Interaction between PAX1, SET1B, histone H3K4 HMT, and DNA demethylases, as detected by co-IP. An anti-FLAG antibody was used for immunoprecipitation, and antibodies against the histone H3K4 HMT complex and DNA demethylases were used for blotting (E). The reverse experiment, i.e., complexes immunoprecipitated by an antibody against WDR5, and immunoblot for Flag (F). (G) The binding of WDR5, within the PTPRR promoter in PAX1-expressing cells, after EGF treatment. Full blots are shown in Supplementary Figs S8 and S9.