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Figure 8 | Epigenetics & Chromatin

Figure 8

From: Protection of CpG islands against de novo DNA methylation during oogenesis is associated with the recognition site of E2f1 and E2f2

Figure 8

E2F1 binding of CpG islands (CGIs) in MCF7 cells is associated with lack of CGI methylation, independent of CGI promoter activity. We fitted a logistic regression model to MCF7-specific data on the methylation state (M in {0, 1}; derived from ENCODE RRBS-seq; see main text), promoter activity (P = log10 of maximum TPM observed by FANTOM5 CAGE) and E2F1 binding (E2F1 in {0, 1}; derived from [32]; see Methods) for 12,358 unmethylated (M = 0) and 4,427 methylated (M = 1) CGIs. All coefficients of the fitted model, M = logit(-1.31 -1.63*P -3.49*E2F1 + 0.60*P*E2F1), were of significant magnitude (P <10-7), that is, promoter activity and E2F1 binding both were independently and significantly negatively associated with CGI methylation, the degree of association being approximately 10x greater for E2F1. All terms of the model, including the interaction term, significantly improved model fit (chi-squared P <10-6). The plot shows the relationship between the level of CGI promoter activity (x-axis) and the probability of the CGI being methylated as predicted by the fitted model (y-axis), separately for CGIs bound by E2F1 (E2F1+) versus for CGIs not bound by E2F1 (E2F1-). The probability is essentially zero for CGIs bound by E2F1, irrespective of the level of their promoter activity, while in the absence of E2F1, the methylation state depends on the level of promoter activity, with only active CGIs (x >0: TPM >1) dropping below the 20% methylation threshold (y <0.2) typically considered as unmethylated.

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