The Pv-CreERT2 (Pvalb-CreERT2) knockin/knockout allele both abolishes parvalbumin (Pvalb; also called PV or Pva) gene function and expresses a CreER^T2 fusion protein (creERT2 fusion protein) from the Pvalb promoter/enhancer elements. Homozygous mice are viable and fertile. Homozygotes are expected to have a knockout phenotype similar to other null mutations of this gene and may exhibit muscle contractile, mitochondrial, and/or Purkinje cell abnormalities. Cre-ERT2 fusion gene activity is inducible; observed following tamoxifen administration. As such, when Pv-CreERT2 mice are bred with mice containing loxP-flanked sequence(s), tamoxifen-inducible Cre-mediated recombination will result in deletion of the floxed sequence(s) in the Pvalb-expressing cells of the offspring.

The donating investigator reports tamoxifen-inducible Cre recombinase activity recapitulates the endogenous Pvalb expression pattern, but with low efficiency of induction. They report tamoxifen-inducible Cre recombinase activity is observed in parvalbumin positive neurons in neocortex and cerebellum, and did not examine cre expression in tissues other than brain.

For characterization information, see images at the Allen Institute for Brain Science website (Pvalb-CreERT2 images).

The Cre-ERT2 fusion protein consists of Cre recombinase fused to a triple mutant form of the human estrogen receptor which does not bind its natural ligand (17β-estradiol) at physiological concentrations but will bind the synthetic estrogen receptor ligands 4-hydroxytamoxifen (OHT or tamoxifen) and, with lesser sensitivity, ICI 182780. Restricted to the cytoplasm, Cre-ERT2 can only gain access to the nuclear compartment after exposure to tamoxifen. To counteract the mixed estrogen agonist effects of tamoxifen injections, which can result in late fetal abortions in pregnant mice, progesterone may be coadministered.