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. 2010 Jan 14;29(4):830–842. doi: 10.1038/emboj.2009.395

Figure 8.

Figure 8

Repression of Bax and Puma is specific through the MAR by SMAR1. (A, B) Luciferase activity of the full-length BAX (plucBax) and MAR-deleted (plucBaxΔMAR) reporters in HCT116 p53+/+ cells treated with low dose 5 J/m2 UV. (C, D) Promoter read out of plucBax and plucBaxΔMAR reporters in HCT116 p53+/+ cells transfected with two different PML siRNAs and analysed 24 h after treatment with high dose UV (100 J/m2). (E) Expression analyses of Bax and Puma on double knockdown of PML and SMAR1 in HCT116 p53+/+ cells. (F) Model showing the MAR element (blue box) of BAX and PUMA promoter juxtaposed to each other causing the looping out of the intervening sequence. SMAR1 (orange) binds to this identical MAR element along with HDAC1 (green) and p53 (red) forming a repressor complex switching off transcription after mild DNA damage (suppression of apoptosis). After severe apoptotic DNA damage, SMAR1 is no longer bound to the MAR element facilitating p53 acetylation (p53-Ac) and transcription of BAX and PUMA (induction of apoptosis).