Jun Dimerization Protein 2 Controls Senescence and Differentiation via Regulating Histone Modification

Figure 1

Schematic representation of the signal pathways of retinoic acid- (RA-) induced (RA-induced) differentiation of mouse embryonic carcinoma F9 cells. At the undifferentiation stage of F9 cells, HDAC3, NcoR/SMART, and JDP2 were recruited on the DRE (differentiation response element) in the promoter region of the c-jun gene to induce the heterochromatin. In the response to retinoic acid (RA), the signals of mitogen-activated kinase (MAPK; phosphorylated (p38(α/β)), BRG1-based SWI/SNF ATPase complex, Ini1/Snf5/SWI/SNF/BAF60 complex, p160 hormone coactivator (RARE/RXRE binding), and p300/PCAF complex were recruited to the DRE element of the c-Jun promoter and then Mediator, Pol II complex (IIB, IIF, IIE, IIH complex), TBP complex, and some TAF complex (ATF12, TAF 4 etc), and recruited and Pol II complex is elongated with phosphorylation of the carboxy terminal domain (CTD) of Pol II, and then c-Jun genes are finally activated. Ac, acetylated residues; K, lysine residues of histone; H3K, lysine residues of histone H3; H4K8, lysine residue at position 8 of histone H4; H4K16, lysine residue at position 16 of histone H4; X1 = ATF-2, ATF-7. JunD, JunB, JDP2, and so forth; X2 = c-Jun and so forth.