Myf5CreER knock-in mice express the CreERTM fusion protein from the endogenous myogenic factor 5 (Myf5) promoter/enhancer elements. MYF5 is expressed during muscle development and is involved in regulating myogenesis. MYF5 is also expressed in a fraction of satellite cells. Homozygotes are viable and fertile. Cre-ERTM fusion gene activity is inducible and can be observed following tamoxifen administration. As such, when these mice are bred with mice containing loxP-flanked sequences, tamoxifen-inducible Cre-mediated recombination will result in deletion of the floxed sequences in muscle cells of the offspring.
For example, when bred to B6.129X1-Gt(ROSA)26Sortm1(EYFP)Cos/J mice (Stock No. 006148), tamoxifen inducible excision of the loxP-flanked STOP sequence results in YFP fluorescence in Myf5-expressing muscle cells of the offspring at different developmental stages.
The Cre-ERTM fusion protein consists of Cre recombinase fused to a G525R mutant form of the mouse estrogen receptor ligand binding domain which fails to bind the naturally occurring ligand 17b-estradiol at normal concentrations but retains relatively high affinity for the synthetic ligand 4-hydroxytamoxifen (4-OHT). Restricted to the cytoplasm, Cre-ERTM 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.
