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. 2022 Aug 9;13:4680. doi: 10.1038/s41467-022-32472-0

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© The Author(s) 2022

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. 6 — a DPF3a, SNIP1, SMAD4, and p300 form in a complex. HA-tagged DPF3a or endogenous SNIP1 protein was immunoprecipitated and followed by immunoblotting using antibodies against SMAD4 and p300 to detect the co-precipitated endogenous SMAD4 and p300. Three independent experiments were performed and similar results were obtained. b SNIP1 bridges DPF3a to SMAD4 and p300. SNIP1 was knocked down in 786-O cells using shRNA. HA-tagged DPF3a protein was immunoprecipitated using anti-HA magnetic beads and followed by immunoblotting using antibodies against SNIP1, SMAD4, and p300 to detect the co-precipitated endogenous SNIP1, SMAD4, and p300. Input lanes represent 5% of total protein lysate. Three independent experiments were performed and similar results were obtained. c Co-occupancy of DPF3a, SNIP1, SMAD4, and p300 on the genome. Average profiles and heatmaps of normalized read density of ChIP-seq for DPF3a, SNIP1, p300, and SMAD4 overlapped peaks (n = 6,921). DPF3a and SNIP1 ChIP-seq data used in this figure are identical to the data used in Fig. 5f. d DPF3a releases SNIP1-mediated inhibition of p300 HAT activity in vitro. In vitro HAT activity assays of p300 in the presence of recombinant full-length SNIP1 (FL) or its N-terminus in combination with full-length DPF3a (FL), its N-terminus or C-terminus. Data were presented as mean values (n = 2 independent experiments). e Overexpression of DPF3a enhances local histone acetylation at specific loci. Pan-H3ac ChIP experiments were performed and H3ac enrichment at selected regions in DPF3a-OE cells was compared to EV control. Enrichment of H3ac was quantified by qPCR. Data were presented as mean values ± SD (n = 3 independent experiments). Statistical significance was estimated using a two-sided student t-test. Source data are provided in the Source Data file.