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. 2018 Oct 13;47(1):152–167. doi: 10.1093/nar/gky947

Figure 6.

Figure 6.

The ability of DNMT3L to interact with DNMT3A2 is critical for DNMT3A2 stability. (A) Co-immunoprecipitation experiment showing that Myc-tagged WT DNMT3L, but not the F297D mutant, interacts with endogenous DNMT3A2. (B) Western blot analysis showing that stable expression of WT DNMT3L, but not the F297D mutant, rescues DNMT3A2 levels in Dnmt3l KO mESCs. Different lanes represent independent clones. (C and D) Analysis of DNMT3A2 protein stability showing that WT DNMT3L, but not the F297D mutant, restores DNMT3A2 stability. Shown are representative blots (C) and quantification of the data (mean ± SD from three independent experiments) by densitometry using ImageJ (D). (E) Southern blot analysis showing that expression of WT DNMT3L, but not the F297D mutant, in Dnmt3l KO mESCs results in recovery of DNA methylation at the major satellite repeats.