Heterozygous Pax3(Cre/+) mice display a white belly spot, as do Splotch heterozygotes.
We have shown that these mice display a cell-autonomous serotonergic wiring phenotype, and have characterized the behavioral consequences.
Consequently, PPARγ+/− mice display a significantly higher bone mass due to increased bone generation (Akune et al., 2004).
Indeed, LAB mice display a deficit in hypothalamic AVP [25].
In addition, the mutant mice display a microphthalmia phenotype.
However, LRP5 knockout mice display a relatively normal vascular network in the ganglion cell layer.
In contrast, the LAMP-2 knockout mice display a more severe phenotype.
Accordingly, TGFβ1-deficient mice display a severe defect in LC, but not in DC, development [21].
AID deficient mice display a mild B cell hyperplasia and enlarged germinal centers [6].
Homozygous prestin knockout mice display a 40 60 dB hearing loss [9].
However, under environmental factors that cause stress, mutant mice display a hypoactive behavior.
