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. 2016 May 15;30(10):1240–1250. doi: 10.1101/gad.279414.116

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© 2016 Lee et al.; Published by Cold Spring Harbor Laboratory Press

This article is distributed exclusively by Cold Spring Harbor Laboratory Press for the first six months after the full-issue publication date (see http://genesdev.cshlp.org/site/misc/terms.xhtml). After six months, it is available under a Creative Commons License (Attribution-NonCommercial 4.0 International), as described at http://creativecommons.org/licenses/by-nc/4.0/.

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Figure 3. — The Bak Q75L mutation renders cells more sensitive to apoptotic stimuli. (A) The killing activity of BH3-only proteins BIM_S (promiscuous prosurvival protein binder) and NOXA (MCL-1-selective) expressed retrovirally in MEFs. The Bak Q75L renders MEFs sensitive to Mcl-1 antagonism. (B) Mitochondria from permeabilized Bak^Q75L/Q75L MEFs have a lower threshold for cytochrome c release than mitochondria from wild-type cells. An approximately fourfold lower concentration of tBIDM97A induced cytochrome c release from pellet (P) containing mitochondria to soluble (S) fractions in Bak^Q75L/Q75L compared with Bak^+/+ MEFs. (C) Mitochondria from Bak^Q75L/Q75L MEFs require a higher (approximately fourfold) concentration of full-length BCL-X_L to inhibit cytochrome c release in response to tBIDM97A (9 nM) treatment. (D–G) MEFs were treated with bortezomib (proteasome inhibitor) (D), actinomycin D (transcription inhibitor) (E), etoposide (topoisomerase inhibitor) (F), or cycloheximide (translation inhibitor) (G) for 24 h prior to measurement of cell viability by FACS following propidium iodide staining. The percent viability is the PI^−ve population in treated cells relative to the same population in cells treated with vehicle (DMSO). Data in A and D–F are presented as mean ± SD of n = 3–4 experiments.