All Phenotypes Wasf2<tm1Tta> MGI Mouse

embryonic lethality during organogenesis, complete penetrance ( J:84651 )

• homozygotes are detected at E10 but show a drastic decline in survival at E10.25-E10.5

• no live homozygotes are recovered at E11.5

abnormal capillary morphology ( J:84651 )

• at the 22 somite stage, vitelline capillaries are small and occasionally discontinous and the general capillary network is occasionally disrupted

abnormal capillary branching pattern ( J:84651 )

• head capillaries are less dense and branched

decreased capillary density ( J:84651 )

• head capillaries are less dense and branched

abnormal intersomitic vessel morphology ( J:84651 )

• 33.3% of homozygotes with 22 somites exhibit disorganized intersomitic vessels

abnormal placental labyrinth vasculature morphology ( J:84651 )

• at the 22 somite stage, homozygotes show impaired angiogenic sprouting in the placental labyrinthine region

abnormal cardiovascular development ( J:84651 )

• homozygotes exhibit defective cardiovascular development due to impaired migration of endothelial cells

abnormal angiogenesis ( J:84651 )

• homozygotes fail to exhibit normal angiogenic remodeling and sprouting in the embryo proper (including the most dorsal part of somites and neural tube), yolk sac and placenta

abnormal dorsal aorta morphology ( J:84651 )

• at the 22 somite stage, major vessels of the trunk (e.g. dorsal aorta and anterior cardinal vein) are relatively small while large vessels of the head fail to develop properly

abnormal anterior cardinal vein morphology ( J:84651 )

• at the 22 somite stage, major vessels of the trunk (e.g. dorsal aorta and anterior cardinal vein) are relatively small while large vessels of the head fail to develop properly

abnormal vascular endothelial cell development ( J:84651 )

• homozygotes show abnormal development of the endothelial lineage in the heart; however, myocardial walls appear relatively normal

• mutant endothelial cells of the aorta and head capillaries appear flatter than normal

• notably, homozygotes exhibit some gaps in the vascular endothelial cells of head capillaries and in endothelium of the heart; leaking erythrocytes and fewer membrane protrusions are also observed

• mutant endothelial cells form cell polarity in response to vascular endothelial growth factor; however, formation of lamellipodia at leading edges and capillaries is severely impaired

failure of heart looping ( J:84651 )

• at E10.5, homozygotes display incomplete cardiac looping

abnormal endocardium morphology ( J:84651 )

• at the 22 somite stage, homozygotes display a less complex ventricular endocardium and a collapsed atrial endocardium

small heart ( J:84651 )

• at E10.5, mutant hearts are small

trabecula carnea hypoplasia ( J:84651 )

abnormal pericardial cavity morphology ( J:84651 )

• at E10.5, homozygotes exhibit dilated pericardial cavities

hemorrhage ( J:84651 )

• at E10.5, 57% of homozygotes exhibit hemorrhages in the head regions, pericardial cavities, hearts and ventral parts of the trunk

hemopericardium ( J:84651 )

intracranial hemorrhage ( J:84651 )

abnormal placental labyrinth vasculature morphology ( J:84651 )

• at the 22 somite stage, homozygotes show impaired angiogenic sprouting in the placental labyrinthine region

embryonic growth retardation ( J:84651 )

• at >E8.5, homozygotes display growth retardation relative to wild-type embryos

decreased embryo size ( J:84651 )

• at E10.5, mutant embryos are significantly smaller than wild-type embryos

incomplete somite formation ( J:84651 )

• at E9.5, homozygotes never contain more than 29 somites whereas wild-type embryos have >30 somites

pale yolk sac ( J:84651 )

• at E10.5, homozygotes are fragile and mutant yolk sacs are pale with few blood cells

abnormal vitelline vascular remodeling ( J:84651 )

• at the 22 somite stage, homozygotes show normal remodeling of the vascular plexus and formation of larger vessels (vitelline arteries and veins); however, capillaries are significantly smaller and occasionally discontinuous