Genetic and epigenetic editing experiments establish causal links between transposon-derived enhancers and gene regulation in mouse embryonic and extraembryonic lineages.

Hundreds of retrovirus-like sequences have features that suggest they might be gene enhancers, but only a small fraction displays gene-regulating activity in experiments on mouse stem cells.

Mice deficient in the TRPM6 channel suffer from impaired prenatal development, shortened lifespan, growth deficit and disturbed energy balance due to a defect in epithelial Mg²⁺ uptake, thus highlighting a pivotal role of TRPM6 in organismal Mg²⁺ homeostasis.

Guidelines governing research into embryos need to be updated in a way that reflects the moral status of synthetic human entities generated using the methods of synthetic biology.

PCGF6 links sequence specific target recognition by the MAX/MGA transcription factor complex to PRC1 (polycomb repressive complex 1) -dependent transcriptional silencing of germ cell-specific genes in mouse pluripotent stem cells.

The reconstitution of a functional envelope protein from an extinct hominid retrovirus reveals its receptor and an ancient host defense that may have led to the extinction of the virus.

Genetic manipulations show that endogenous transcription factors of the SoxB1 class act redundantly to maintain primed pluripotency and reveal differential effects on transitions between pluripotent and differentiation states.

Lineage specification and commitment are synchronized in the developing trophectoderm lineage of the mouse embryo, but are asynchronous events in the maturing inner cell mass, revealing a window of plasticity in this lineage.

A previously unrecognized transcriptional coactivator function of the dyskerin ribonucleoprotein complex and its associated small nucleolar RNA has been uncovered and mediates embryonic stem cell-specific transcription.

At gastrulation, mesoderm arises as a migratory germ layer that will participate to both foetal and placental development through region-dependant adaptation of cytoskeleton composition, cell shape and migration mode.