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Background  Histone methylation is thought to be central to the epigenetic mechanisms that maintain and confine cellular identity in multi-cellular organisms. To examine epigenetic roles in cellular homeostasis, we conditionally mutated the histone 3 lysine 4 methyltransferase, Mll2, in embryonic stem (ES) cells, during development and in adult mice using tamoxifen-induced Cre recombination.    Results  In ES cells, expression profiling unexpectedly revealed that only one gene,  Magoh2 , is dependent upon Mll2 and few other genes were affected. Loss of Mll2 caused loss of H3K4me3 at the  Magoh2  promoter and concomitant gain of H3K27me3 and DNA methylation. Hence Mll2, which is orthologous to  Drosophila  Trithorax, is required to prevent Polycomb-Group repression of the  Magoh2  promoter, and repression is further accompanied by DNA methylation. Early loss of Mll2  in utero  recapitulated the embryonic lethality found in  Mll2 -/- embryos. However, loss of Mll2 after E11.5 produced mice without notable pathologies. Hence Mll2 is not required for late development, stem cells or homeostasis in somatic cell types. However it is required in the germ cell lineage. Spermatogenesis was lost upon removal of Mll2, although spermatogonia A persisted.    Conclusion  These data suggest a bimodal recruit and maintain model whereby Mll2 is required to establish certain epigenetic decisions during differentiation, which are then maintained by redundant mechanisms. We also suggest that these mechanisms relate to the epigenetic maintenance of CpG island promoters.

The histone 3 lysine 4 methyltransferase, Mll2, is only required briefly in development and spermatogenesis