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. 2010 Jul 27;285(39):29842–29850. doi: 10.1074/jbc.M110.116319

FIGURE 3.

FIGURE 3.

YY1 bound to the regulatory region of ChM-I and decreased the promoter activity of ChM-I. A, ChIP-qPCR assay for YY1 and HDAC2. B, luciferase reporter assay. a, DNA fragment encompassing −446 to +86 was cloned into a reporter vector containing the luciferase gene (PGV-B-f1). The black box indicates the location of the consensus sequence for the YY1-binding motif. b, PGV-B-f1-mt contains mutations in the YY1-binding motif (arrowhead), and PGV-B-f1-del lacked the YY1-binding motifs (c). Each reporter vector was co-transfected with empty vector (pCEP) or the YY1 expression vector (pCEP-YY1) into ANOS. The fold-increase was calculated based on empty vector activity. C, expression of endogenous ChM-I in hPCs transfected with the YY1 expression vector. The expression of ChM-I was semi-quantified taking the value for endogenous expression as 1.0 and is demonstrated at the top. D, ChIP-qPCR assay of hPCs transfected with the YY1 expression vector with or without MS275 treatment (1 μm for 24 h). Forced expression of YY1 in hPCs changed the modification of the H3 tail from acetylation to dimethylation.