A cysteine to arginine amino acid substitution at residue 179 (R179C) of the Gnai2 sequence interferes with the ability of the mutant protein to hydrolyze GTP, rendering it constitutively active. This mutant form of the gene was placed under the control of the tetO promoter in these transgenic mice. A second construct expressing bacterial beta-galactosidase (lacZ) under the regulation of a tetO promoter was coinjected with the Gnai2 vector. (J:109030)
Legend:
cx: complex: > 1 genome feature ot: other: hemizygous, indeterminate,... (F): Female
(M): Male
N: normal phenotype
(#): related diseases count