The imprinted gene finely tunes control of feeding and growth in neonates.

Genomic imprinting refers to the mono-allelic and parent-specific expression of a subset of genes. While long recognized for their role in embryonic development, imprinted genes have recently emerged as important modulators of postnatal physiology, notably through hypothalamus-driven functions. Here, using mouse models of loss, gain and parental inversion of expression, we report that the paternally expressed gene controls neonatal growth in mice, in a dose-sensitive but parent-of-origin-independent manner.

Effects of assisted reproductive technologies on transposon regulation in the mouse pre-implanted embryo.

Study Question: Do assisted reproductive technologies (ARTs) impact on the expression of transposable elements (TEs) in preimplantation embryos?

Summary Answer: The expression of all TE families is globally increased with mouse embryo culture with differences according to culture medium composition.

What Is Known Already: Mammalian genomes are subject to global epigenetic reprogramming during early embryogenesis. Whether ARTs could have consequences on this period of acute epigenetic sensitivity is the matter of intense research.

Persistent cell migration and adhesion rely on retrograde transport of β(1) integrin.

Integrins have key functions in cell adhesion and migration. How integrins are dynamically relocalized to the leading edge in highly polarized migratory cells has remained unexplored. Here, we demonstrate that β1 integrin (known as PAT-3 in Caenorhabditis elegans), but not β3, is transported from the plasma membrane to the trans-Golgi network, to be resecreted in a polarized manner.

Plasticity in Dnmt3L-dependent and -independent modes of de novo methylation in the developing mouse embryo.

A stimulatory DNA methyltransferase co-factor, Dnmt3L, has evolved in mammals to assist the process of de novo methylation, as genetically demonstrated in the germline. The function of Dnmt3L in the early embryo remains unresolved. By combining developmental and genetic approaches, we find that mouse embryos begin development with a maternal store of Dnmt3L, which is rapidly degraded and does not participate in embryonic de novo methylation.

Protection against de novo methylation is instrumental in maintaining parent-of-origin methylation inherited from the gametes.

Identifying loci with parental differences in DNA methylation is key to unraveling parent-of-origin phenotypes. By conducting a MeDIP-Seq screen in maternal-methylation free postimplantation mouse embryos (Dnmt3L-/+), we demonstrate that maternal-specific methylation exists very scarcely at midgestation. We reveal two forms of oocyte-specific methylation inheritance: limited to preimplantation, or with longer duration, i.

Nodal cis-regulatory elements reveal epiblast and primitive endoderm heterogeneity in the peri-implantation mouse embryo.

Nodal, a secreted factor known for its conserved functions in cell-fate specification and the establishment of embryonic axes, is also required in mammals to maintain the pluripotency of the epiblast, the tissue that gives rise to all fetal lineages. Although Nodal is expressed as early as E3.5 in the mouse embryo, its regulation and functions at pre- and peri-implantation stages are currently unknown.