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. 2018 Oct 2;8:14689. doi: 10.1038/s41598-018-32942-w

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© The Author(s) 2018

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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Tet1 L897 and L900 are key residues for interaction with Sin3A in cells. (A) Co-immunoprecipitation followed by western blotting reveals the requirement of L897 and L900 for the interaction with endogenous Sin3A in mouse ES cells. This image is cropped, the uncropped version of the blot is shown in Supplementary Fig. S5D. (B) Transcription of a luciferase reporter assay is driven by a simple TATA based promoter enhanced by addition of a LexA-VP16 fusion protein. Transcription can be repressed by co-expression of either the Mxd1-SID (MadN35), or Tet1-SID fused to a Gal4 DNA binding domain (DBD). Repression is dependent upon the interaction with Sin3A, since mutation of the Tet1-SID causes loss of repression.