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. 2017 Jun 14;7:3473. doi: 10.1038/s41598-017-03152-7

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© The Author(s) 2017

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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Knockdown of HDAC3 increases GATA6/Sp1/p300 interactions. Representative co-immunoprecipitation (co-IP) of cell lysate from MLE-15 cells transduced with Hdac3 shRNA or non-silencing shRNA (NS) demonstrates decreased HDAC3/Sp1 interaction (A), increased GATA6/Sp1 and GATA6/p300 (B), and increased p300/Sp1 (C) interaction following HDAC3 knockdown. n = 3. (D) Model of Sp1-mediated Aqp5 transcriptional regulation and involvement of HDAC3, GATA6, and p300: HDAC3 and GATA6 regulate Sp1-mediated Aqp5 transcription via H3 deacetylation and acetylation, respectively, at the proximal promoter/enhancer. Mechanisms underlying GATA6-dependent H3 acetylation at the Aqp5 enhancer/promoter might involve competition between GATA6 and HDAC3 for binding to Sp1, as well as recruitment of histone acetylase p300 to the Sp1/GATA6 complex. In addition to effects on H3 acetylation, p300 might also modulate GATA6 and/or Sp1 activity.