PT - JOURNAL ARTICLE AU - Mo-bin Cheng AU - Xue Wang AU - Yue Huang AU - Ye Zhang TI - Heat shock induces the depletion of Oct4 in mouse blastocysts and stem cells AID - 10.1101/264044 DP - 2018 Jan 01 TA - bioRxiv PG - 264044 4099 - http://biorxiv.org/content/early/2018/02/12/264044.short 4100 - http://biorxiv.org/content/early/2018/02/12/264044.full AB - Temperature is an important microenvironmental factor that functions epigenetically in normal embryonic development. However, the effect of heat shock in the stem cells is not fully understood. Oct4 is a tightly regulated master regulator of pluripotency maintenance in stem cells and during early embryonic development. We report here that Oct4 protein level was significantly reduced under heat shock in mouse blastocysts and embryonic stem cells. The reduction in Oct4 in the mouse embryonic stem cells under heat shock was mediated by a ubiquitin-proteasome pathway that was dependent on the activity of death- associated protein kinase 1 (Dapk1) to phosphorylate its substrate, Pin1. Our results imply that the depletion of Oct4 via brief heat shock, such as a high fever, during early pregnancy might severely impair the growth of the mammalian embryo or even cause its death.