All Phenotypes Bcar1<tm1Hhi> MGI Mouse

embryonic lethality during organogenesis, complete penetrance ( J:48967 )

• homozygous null embryos die at E11.5-E12.5

blood vessel congestion ( J:48967 )

• at E11.5-E12.5, homozygous null embryos obtained by caesarian section display systemic congestion

abnormal myocardial fiber morphology ( J:48967 )

• mutant cardiocytes exhibit disorganized myofibrils and disrupted Z-disks

thin myocardium ( J:48967 )

abnormal heart development ( J:48967 )

• homozygous null embryos show a poorly developed heart

decreased cardiac muscle contractility ( J:48967 )

• findings suggested that disruption of contractile structures resulted in cardiac pump failure and venous dilatation, leading to low blood pressure, systemic hypoxia and embryonic death

increased vasodilation ( J:48967 )

• homozygous null embryos display significantly dilated blood vessels that retain blood cells

embryonic growth retardation ( J:48967 )

• at E11.5-E12.5, homozygous null embryos obtained by caesarian section exhibit growth retardation

abnormal cell morphology ( J:48967 )

• homozygous null primary fibroblasts appear flat, thin and round-shaped relative to wild-type fibroblasts

• wild-type fibroblasts display thick, dense and long actin bundles traversing the cells; in contrast, mutant fibroblasts exhibit thin, short and irregularly assembled actin filaments at the cell periphery

• transient re-expression of the targeted gene in mutant fibroblasts restores actin stress fiber formation

abnormal cell physiology ( J:48967 )

• expression of activated Src in homozygous null primary fibroblasts fails to induce a fully-transformed phenotype, probably due to limited actin aggregation in podosomes

small liver ( J:48967 )

• at E11.5-E12.5, the mutant liver is occasionally smaller in size; however, no obvious differences are observed in other organs (including CNS, lungs, kidneys and skeletal muscles) at this stage