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Background  Polycomb repressive complex 2 (PRC2) is responsible for establishing and maintaining histone H3K27 methylation during cell differentiation and proliferation. H3K27 can be mono-, di-, or trimethylated, resulting in differential gene regulation. However, it remains unknown how PRC2 specifies the degree and biological effects of H3K27 methylation within a given cellular context. One way to determine PRC2 specificity may be through alternative splicing of  Ezh2 , PRC2’s catalytic subunit, during cell differentiation and tissue maturation.    Results  We fully characterized the alternative splicing of  Ezh2  in somatic cells and male germ cells and found that  Ezh ’s exon 14 was differentially regulated during mitosis and meiosis. The  Ezh2  isoform containing exon 14 (ex14- Ezh2 ) is upregulated during cell cycle progression, consistent with a role in maintaining H3K27 methylation during chromatin replication. In contrast, the isoform lacking exon 14 (ex14D- Ezh2 ) was almost exclusively present in spermatocytes when new H3K27me2 is established during meiotic differentiation. Moreover,  Ezh2 ’s transcript is normally controlled by E2F transcription activators, but in spermatocytes,  Ezh2 ’s transcription is controlled by the meiotic regulator MYBL1. Compared to ex14-EZH2, ex14D-EZH2 has a diminished efficiency for catalyzing H3K27me3 and promotes embryonic stem cell differentiation.    Conclusions   Ezh2 ’s expression is regulated at transcriptional and post-transcriptional levels in a cellular context-dependent manner. EZH2 variants determine functional specificity of PRC2 in histone methylation during cell proliferation and differentiation.    Electronic supplementary material  The online version of this article (10.1186/s13072-018-0242-9) contains supplementary material, which is available to authorized users.

EZH2 variants differentially regulate polycomb repressive complex 2 in histone methylation and cell differentiation