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. 2018 Aug 20;8:12434. doi: 10.1038/s41598-018-30603-6

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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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Deletion of the transmembrane-domain of Bax, Bak or Bok reduces the number of (A) apoptotic (Annexin-V-APC positive) and (B) cells with lost ΔΨm (TMRE^low) in the presence (WT) and absence (DKO) of Bax&Bak. (C) Mutation of the conserved lysine residue in the BH3-domain reduces Bax-induced apoptosis, abolishes Bak-induced apoptosis but has no significant impact on Bok-induced apoptosis in the presence and absence of endogenous Bax&Bak. (D) The number of cells with lost mitochondrial membrane potential is slightly reduced by Bax(L63E), heavily reduced by BakL78E but unchanged by Bok(L70E) both, in HCT116/WT and HCT116/DKO. (E) Combined mutation of the BH3-domain and deletion of the transmembrane-domain severely dampens apoptosis induction by Bax(L63E)ΔTM and Bak(L78E)ΔTM but enhances cell death induction by Bok(L70E)ΔTM. (F) Bax(L63E)ΔTM and Bak(L78E)ΔTM are almost incapable to induce loss of ΔΨm whereas the number of TMRE^low cells is increased in case of Bok(L70E)ΔTM irrespective of the presence (WT) or absence (DKO) of Bax and Bak.