Ablation of Max expression induces meiotic onset in sexually undifferentiated germ cells

MAX (MYC Associated Factor X) is generally known as a mandatory partner for MYC transcription factor, which activates various genes involved in cell growth and metabolism. On the other hand, MAX, when interacting with MGA, forms the polycomb repressive complex (PRC) 1.6, one of the subtypes of PRC1, which directs the transcriptionally repressed chromatin state. Although physiological significance is not known at present, we have previously demonstrated that mouse embryonic stem cells (ESCs) bear a potential to onset meiosis, albeit not germ cells, and PRC1.6 prevent ESCs from their ectopic onset of meiosis (Suzuki et al., 2016, Nat. Commun. 7:11056 doi: 10.1038/ncomms11056). In this study, we aimed to investigate the role of Max in germ cells in vivo by performing the primordial germ cell-specific knockout of the Max gene. Homozygous Max gene-floxed mouse embryos with or without CreERT2 transgene that carries distal enhancer of Oct4 gene were generated by the intercross between Max floxed male mouse with CreERT2 transgene and female Max floxed female mouse without the transgene. Tamoxifen was intraperitoneally administered at E8.5. Genital ridges of tamoxifen-treated male and female embryos were isolated at E12.5. Germ cells recovered from them by means of magnetic-activated cell-sorter (MACS) system were used for RNA sources. These RNAs were used to examine the alteration in global expression profiles due to Max gene disruption in germ cells by DNA microarray analyses. RNAs from homozygous floxed male and female germ cells without CreERT2 transgene were used as reference samples.