Deletion of Shh, Wnt5a or Bmp7 in mouse embryos resulted in reduced proliferation of the urs mesenchyme, incomplete urs elongation and septation defects.
Loss of DLK-1+ hepatoblasts in Map2k4−/− mouse embryos resulted in decreased numbers of hematopoietic cells in fetal liver (Sugiyama et al., 2011b).
Hepatocyte-specific deletion of PR-SET7 in mouse embryos resulted in G2 phase arrest followed by massive cell death and defect in liver organogenesis.
This apparent discrepancy could be due to compensation by the p53 family members p63 and p73, which are expressed in early mouse embryos, resulting in the incomplete penetrance of the developmental phenotype observed.
For example, alcohol consumption by the mother altered DNA methylation profiles in mouse embryos, resulting in neurofacial deficits and growth retardation, both of which are hallmarks of FASD (Liu et al. 2009).
Overexpression of Dvl, a downstream target of Prickle1, Vangl, and Frizzled (Fz) (Gómez-Orte et al., 2013; Lapébie et al., 2011), has been shown to dramatically alter the morphology and adhesion properties of 4-cell stage mouse embryos, resulting in a lack of coherence in the resulting blastocyst (Na et al., 2007).
Loss of Pofut1 in the mouse embryo resulted in a severe phenotype similar to that of embryos lacking core components of Notch signaling pathway, such as Presenilins and Rbpj [10], [11], [12].
Interestingly, inactivation of both RARα and RARβ in mice embryos resulted in renal malformations [ 155].
Homozygous deletion of either Pdgfb or Pdgfrb in mouse embryos results in a complete lack of brain pericytes and CNS microhemorrhages, causing embryonic lethality (Daneman et al., 2010).
Complete deficiency of ADNP in mouse embryos results in changes in gene expression profile [45].
Dubrulle and Pourquié [3] found that the gradient of FGF8 protein, present during somitogenesis in chick and mouse embryos, results from a gradient of FGF8 mRNA transcripts.
