Loss of a maternally inherited epigenetic modifier leads to establishment of an aberrant regulatory network in preimplantation embryos, developmental delay and destabilisation of cell-fate choices.

During mouse preimplantation development, the complete loss of actomyosin contractility abolishes cytokinesis but not apico-basal polarisation, lineage specification, or fluid accumulation, which are the critical steps to the formation of the blastocyst.

Single embryo RNA-seq combined with mouse genetics provides a comprehensive view on the roles of Rlim and Xist for the regulation of X-linked gene expression during early mouse embryogenesis.

The Notch signaling pathway drives transitions in differentiation capacities during the gradual loss of potency that occurs in the preimplantation mouse embryo before the onset of the first lineage decisions.

Identifying the pathways that support human naive-state pluripotent stem cells provides insights into the signalling-based regulation of human pluripotency and enables informed decisions to improve conditions for pluripotent cell culture.

Cyclic estrogen signaling in oviduct epithelial cells suppresses oviduct luminal protease activity to allow survival and development of preimplantation embryos

Analysis of mouse zygotic genome activation (ZGA) reveals that a mis-annotated multicopy homeobox gene Obox4 functions redundantly with Dux to promote ZGA.

Zona pellucida requires ZP4 protein to efficiently protect the developing embryo during in vivo pre-implantation development.

The maternally provided histone demethylase LSD1/KDM1A has an instrumental role at the beginning of life, shaping the histone methylation landscape and the transcriptional repertoire of the early mouse embryo.