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. Author manuscript; available in PMC: 2012 May 6.
Published in final edited form as: Mol Cell. 2011 May 6;42(3):342–355. doi: 10.1016/j.molcel.2011.04.011

Figure 7.

Figure 7

OCA-B requirement for endogenous Igh expression in primary B cells. (A) Cellular populations from NP-immunized Oca-b+/+ and Oca-b−/− splenocytes were analyzed by FACS using antibodies against the indicated cell surface markers. (B) VH186.2 mRNA levels in Oca-b+/+ and Oca-b−/− splenocytes were analyzed by quantitative RT-PCR after normalization to Gapdh mRNA. Results are presented as the mean ± SD. (C) Effects of OCA-B on Igh promoter-enhancer interactions in wild type and OCA-B null primary cells were measured by 3C as described in Methods. After HindIII digestion, all Igh genes containing JH2 or JH3 segments after VDJ recombination were analyzed. (D) A proposed model for OCA-B and TFII-I interaction that facilitates Igh promoter and HS4 enhancer communication. First, binding of OCA-B to promoter-bound TFII-I relieves HDAC3 binding and the associated repression. Second, an interaction between enhancer-bound OCA-B and TFII-I facilitates juxtaposition, by looping, between Igh promoter and enhancer elements. Proper enhancer function is achieved by facilitated factor recruitment to the promoter and/or by a direct transfer mechanism.