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. Author manuscript; available in PMC: 2010 May 1.
Published in final edited form as: J Mol Cell Cardiol. 2009 Jan 21;46(5):621–635. doi: 10.1016/j.yjmcc.2009.01.005

Figure 3. Transcription driven by the 0.44 kb SM22α promoter is stimulated by Wnt3a, alone and in concert with TGFβ1.

Figure 3

Figure 3

Figure 3

Figure 3

Figure 3

Figure 3

Figure 3

Figure 3

Panel A, C3H10T1/2 cells were transiently transfected with 441 SM22LUC, a construct possessing SM22α promoter region −441 to +5 upstream of the LUC reporter of plasmid pGL2, and treated with vehicle, Wnt3a (15 ng/ml), TGFβ1 (5 ng/ml) and/or Wnt5a (30 ng/ml) as indicated. Panel B, addition of nucleotide +5 to +44, encompassing although augmenting basal activity, the novel exon 1 SBE(43), increased basal activity but was not required for Wnt3a responsiveness. Wnt3a (15 ng/ml, 5 hours) treatment increased SM22α histone H3 acetylation (panel C) and β-catenin binding (panel D) in ChIP assay, confirming transcriptional activation. Panels E & F, a SM22α promoter 5′-deletion series was analyzed to map the Wnt3a response between nucleotides −213 and −190. Panel G, concatamers of 3- and 6-copy direct repeats of SM22α promoter region −213 to −192 conveyed Wnt3a + TGFβ1 responsiveness onto the unresponsive RSV minimal promoter of RSVLUC. Panel H, a single copy of SM22α[ −213/−192] can convey Wnt3a responsiveness to the RSV promoter.