Skip to main content
. Author manuscript; available in PMC: 2016 Mar 17.
Published in final edited form as: Nat Med. 2015 Mar;21(3):212–213. doi: 10.1038/nm.3815

Figure 1.

Figure 1

The role of DNA methylation in osteoclast differentiation. RANKL is a regulator of osteoclastogenesis. Nishikawa et al.7 show in mouse osteoclast precursor cells that it induces the expression of the de novo DNA methyltransferase Dnmt3a and increases oxidative metabolism to provide the SAM substrate for Dnmt3a. After RANKL-induced signaling, the expression of Irf8, a negative regulator of osteoclastogenesis is repressed. Dnmt3a maintains this repression by methylating CpG motifs in putative regulatory elements downstream of the Irf8 gene body, thereby promoting osteoclast differentiation and bone resorption. RANK, receptor activator of NF-κB.