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Trimethylation on H3K27 mediated by Polycomb Repressive Complex 2 (PRC2) is required to control gene repression programs involved in development, regulation of tissue homeostasis or maintenance and lineage specification of stem cells. In  Drosophila , the PRC2 catalytic subunit is the single protein E(z), while in mammals this function is fulfilled by two proteins, Ezh1 and Ezh2. Based on database searches, we propose that  Ezh1  arose from an  Ezh2  gene duplication that has occurred in the common ancestor to elasmobranchs and bony vertebrates. Expression studies in zebrafish using  in situ  hybridization and RT-PCR followed by the sequencing of the amplicon revealed that  ezh1  mRNAs are maternally deposited. Then,  ezh1  transcripts are ubiquitously distributed in the entire embryo at 24 hpf and become more restricted to anterior part of the embryo at later developmental stages. To unveil the function of  ezh1  in zebrafish, a mutant line was generated using the TALEN technology. Ezh1-deficient mutant fish are viable and fertile, but the loss of  ezh1  function is responsible for the earlier death of  ezh2  mutant larvae indicating that  ezh1  contributes to zebrafish development in absence of zygotic  ezh2  gene function. Furthermore, we show that presence of  ezh1  transcripts from the maternal origin accounts for the delayed lethality of  ezh2 -deficient larvae.

Ezh1 arises from Ezh2 gene duplication but its function is not required for zebrafish development