The T-box18 gene (Tbx18) encodes a transcription factor that functions in embryonic development, and is a marker of proepicardial cells (PEs) and epicardium. PEs generate cardiac fibroblasts, smooth muscle cells (SMCs) and endothelial cells that form coronary arteries. Tbx18 is actively expressed in vascular support cells (pericytes and vascular SMCs), and is involved in the development of pacemaker cells. TBX18 specifically marks dermal papilla precursor cells during embryonic hair follicle morphogenesis. 
 The Tbx18-CreERT2 knock-in/knock-out allele has a tamoxifen-inducible Cre recombinase fusion gene (CreERT2) inserted six bp upstream of the endogenous Tbx18 translation initiation codon. This allele is also called Tbx18CreERT2 or Tbx18ERT2Cre. 
 The donating investigator reports there is no Cre recombinase activity prior to tamoxifen exposure. Heterozygous mice are viable and fertile with no reported gross physical or behavioral abnormalities. Homozygous mice are TBX18 null - exhibiting shortened body length and postnatal death due to severe skeletal and respiratory failure (complete penetrance). 
 When Tbx18-CreERT2 mice are bred with mice containing lox-flanked (floxed) sequences, tamoxifen-inducible Cre-mediated recombination will result in deletion of floxed sequences in Tbx18-expressing cells of the offspring. Specifically, tamoxifen-inducible Cre recombinase activity recapitulates the endogenous Tbx18 expression pattern. For example, Tbx18-CreERT2 mice allow for high-efficiency, time-controlled, genetic labeling of pericytes and vascular smooth muscle cells in intact tissues. When Tbx18-CreERT2 are bred to have the Cre-inducible tdTomato reporter allele Ai9 (Stock Nos. <a href="https://www.jax.org/strain/007905">007905</a>/<a href="https://www.jax.org/strain/007909">007909</a>), the resulting tamoxifen-treated double mutant mice show robust and reproducible labeling of more than 90% of pericytes and 85% of vascular smooth muscle in brain, heart, and brown and white fat depots. Highly efficient labeling of the membranous linings of the brain and heart, pia mater and epicardium was also observed. Tbx18-CreERT2 lineage-traced cells did not co-localize with neuronal or glial markers in the brain, nor cardiomyocyte markers in the heart. 
 The CreERT2 fusion protein consists of Cre recombinase fused to a triple mutant form of the human estrogen receptor that does not bind its natural ligand (17&beta;-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, CreERT2 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 co-administered.

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Tbx18-CreERT2 knock-in/knock-out has the endogenous T-box18 promoter/enhancer sequences directing expression of tamoxifen-inducible Cre recombinase. These mice allow specific and inducible genetic manipulations in vivo for studying pericytes and vascular smooth muscle cells in multiple tissues, as well as proepicardium/epicardium cell lineages and pacemaker cells of the sino-atrial node.

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