Analysis Tools
mortality/aging
|
• genotyping of animals that survived after weaning showed that only 8.7% were homozygous null mutants
|
|
• at birth, homozygous null mice were viable and appeared grossly normal; however, approximately 47% of them died within 24 hours after birth
|
craniofacial
| N |
• at E16.5, development of other oral structures, including the mandible, the tongue, the molar teeth, the incisor teeth, and the Meckel's cartilage, all appeared normal in homozygous null embryos
|
|
• skeletal staining of the homozygous null skull revealed that initial formation and elevation of the palatal shelves proceeded properly
• however, the palatal bones in the homozygous mutant animals often failed to extend toward the midline at the base of the skull and fuse properly, resulting in a cleft of the palate
|
|
• at E18.5, 60% of homozygous null mutants displayed a cleft secondary palate
• all homozygous null mice that died after birth had a complete cleft of the secondary palate; in contrast, the secondary palate in homozygous null mice that survived appeared normal
|
nervous system
|
• basal telencephalic cholinergic neurons were born but failed to differentiate properly in homozygous null mice
|
|
• adult homozygous null mice lacked multiple types of telencephalic cholinergic neurons, including hippocampal and cortical projection neurons in the septum and nucleus basalis, respectively, and local circuit neurons in the striatum
• in addition, the number of cholinergic neurons was decreased in areas of the subcortical forebrain, including the caudate-putamen, medial septal nucleus, nucleus of the diagonal band, and magnocellular preoptic nucleus
• although mutants failed to generate most of the cholinergic neurons in the basal telencephalon, some subsets were still produced e.g. the cholinergic interneurons in the ventral striatum (e.g. the nucleus accumbens) and the parvocellular component of the cholinergic magnocellular preoptic nucleus
|
digestive/alimentary system
|
• skeletal staining of the homozygous null skull revealed that initial formation and elevation of the palatal shelves proceeded properly
• however, the palatal bones in the homozygous mutant animals often failed to extend toward the midline at the base of the skull and fuse properly, resulting in a cleft of the palate
|
|
• at E18.5, 60% of homozygous null mutants displayed a cleft secondary palate
• all homozygous null mice that died after birth had a complete cleft of the secondary palate; in contrast, the secondary palate in homozygous null mice that survived appeared normal
|
growth/size/body
|
• skeletal staining of the homozygous null skull revealed that initial formation and elevation of the palatal shelves proceeded properly
• however, the palatal bones in the homozygous mutant animals often failed to extend toward the midline at the base of the skull and fuse properly, resulting in a cleft of the palate
|
|
• at E18.5, 60% of homozygous null mutants displayed a cleft secondary palate
• all homozygous null mice that died after birth had a complete cleft of the secondary palate; in contrast, the secondary palate in homozygous null mice that survived appeared normal
|
reproductive system
 |
• P0 ovaries show significant downregulation of oogenesis-related genes including genes involved in in early folliculogenesis (Figla, Nobox, Lhx8, Sohlh2, Kit, Ybx2, Gdf9, Jag1, Jag2); however, no downregulation of Sohlh1 or Taf4b is observed
• FIGLA protein is undetectable in oocytes while the abundance of SOHLH2, NOBOX and KIT proteins is severely reduced in oocytes at P0
|
cellular
|
|
• P0 ovaries show significant downregulation of oogenesis-related genes including genes involved in in early folliculogenesis (Figla, Nobox, Lhx8, Sohlh2, Kit, Ybx2, Gdf9, Jag1, Jag2); however, no downregulation of Sohlh1 or Taf4b is observed
• FIGLA protein is undetectable in oocytes while the abundance of SOHLH2, NOBOX and KIT proteins is severely reduced in oocytes at P0
|
