Fig. 5: CEBPE inhibits G2/M progression by repression of E2F target gene expression.

a Expression profiles of Nfyb and Lin54 during granulocytic differentiation (mean; whiskers represent the standard error) (N = 3 (LSK), 3 (preGM), 3 (GMP), 6 (GP), 2 (PM), 3 (MY1), 3 (MY2), 3 (MM), 3 (BC), and 3 (GR), biological replicates). b PCA plot showing similar binding profiles for CEBPE, NFYB, and E2F1, but not for MYC and LIN54, at promoters of G2/M genes, as inferred by the ChIP-seq binding signal and binding motif scores. c Cluster B(MY) genes, including G2/M phase genes, were divided into gene subclasses based on the combinatorial binding of four TFs (CEBPE = C, E2F1 = E, NFYB = N, LIN54 = L) (N > 30). CENL subclass (orange): Binding of all four TF. CE subclass (green): Binding of C and E with or without additional binding of either N or L. Rest (blue): Binding of other TF combinations of C, E, N, L, or none of these. Cebpe KO mice demonstrated marked upregulation of genes whose promoters were bound by all the four TFs (i.e., CENL-bound genes). In contrast, CE-bound and the “Rest” group of genes exhibited minimal upregulation in Cebpe KO vs. Cebpe WT mice. The percentages of genes from each TF binding subclass are depicted in brackets. d Functional gene categories enriched among genes from TF binding subclasses. e, f Genome browser view of two key G2/M phase regulators, Ccnbb 4 (e) and Cdk1 (f) bound by all four TFs at their promoters (CENL subclass) in WT and Cebpe KO mice (only CEBPA). Source data are provided as a Source Data file.