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. 2012 Mar 19;196(6):689–698. doi: 10.1083/jcb.201201077

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© 2012 Byrd et al.

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Figure 5. — miR-30c-2* influences the fate of cells challenged with ER stress. (A and B) HeLa cells stably expressing either an miR-30c-2*–specific inhibitor (anti–miR-30c-2*) or a control scrambled inhibitor (Inh Ctrl) were left untreated or treated with Tm for the indicated intervals, stained with 7-AAD, and analyzed by flow cytometry. (A) Histograms discriminating viable (7-AAD negative [Neg]) from dead (7-AAD positive [Pos]) cells. (B) Quantitative analysis of 7-AAD–positive cells during Tm-induced ER stress. Note that anti–miR-30c-2* provided measurable improvement in the viability of untreated cells (0 h), consistent with basal UPR signaling and XBP1(S) expression under these conditions (Fig. 4 D, top). (C and D) XBP1^WT (wild-type [WT]) and XBP1^−/− (knockout [KO]) MEFs transiently expressing either anti–miR-30c-2* or a control scrambled inhibitor were left untreated or treated with Tm for the indicated intervals and analyzed as in A. (C) Histograms discriminating viable (7-AAD negative) from dead (7-AAD positive) cells. (D) Quantitative analysis of 7-AAD–positive cells during Tm-induced ER stress. (E) Model for miR-30c-2* as a regulatory interface between the PERK and IRE1–XBP1 pathways in the UPR, regulating XBP1 expression, the strength of XBP1-mediated gene transcription, and cellular adaptation to ER stress. Data are means ± SD. *, P < 0.05. P, phospho.