Prx1 cre

The Dermo1-Cre, Prx1-Cre, UBC-CreERT2, and Trp53^f/f mice were obtained from Jackson Lab and maintained by breeding with WT C57BL/6 strains. The Senp6 floxed mice were created by the laboratory of Dr. Edward Yeh and maintained on C57BL/6 background. Mice at embryonic or perinatal stages were not separated by sexes. The mice at p12, p21, and adult age used in the present study were males. The littermates were randomly grouped based on genotypes for all the experiments. The animal procedures were approved by the Van Andel Research Institute Animal Care and Use Committee.

The following mouse lines were used: Fzd2^fl (Kadzik et al., 2014 (link)), Prx1-Cre (The Jackson Laboratory, strain #005584) and K14-Cre (The Jackson Laboratory, strain #018964). All mice were maintained on a mixed strain background. Mice were allocated to experimental or control groups according to their genotypes, with control mice being included in each experiment. Male mice carrying Prx1-Cre were crossed with Fzd2^fl/fl females to avoid potential germ line recombination. Mice were included in the analysis based on their genotypes. Mice were not randomized, as genotype information was required to assign them to control and experimental groups. Investigators were aware of genotype during allocation and animal handling as this information was required for appropriate allocation and handling. Immunostaining and ISH studies were carried out, and data were recorded in a manner that avoided observer bias. Up to five mice were maintained per cage in a specific pathogen-free barrier facility on standard rodent laboratory chow (Purina, 5001). All animal experiments were performed under approved animal protocols according to institutional guidelines established by the Icahn School of Medicine at Mount Sinai IACUC committee.

Mice included in this study were purchased from the Jackson Laboratory (Prx1cre, stock no.005584, Osx-GFP::cre, stock no. 006361, Ror2 ^flox/flox, stock no. 018354). All mice analyzed had a C57BL/6 background. Animals were maintained under specific pathogen-free conditions in the institutional animal facility of the Sun Yat-sen University. All animal studies were performed with a protocol approved by the Animal Ethical and Welfare Committee of Sun Yat-sen University (SYSU-IACUC- 2021001878).

Tek-Cre⁺ (stock no. 008863), Prx1-Cre⁺ (stock no. 005584) and Ubc-Cre-ERT2⁺ (Ubc-Cre⁺) (stock no. 007001) mice were procured from Jackson Laboratory. Cxcl12^f/f mice (loxP sites flanking exon 2) were crossed with Tek-Cre⁺, Prx1-Cre⁺ and Ubc-Cre⁺ mice to generate Cxcl12^f/f-Tek-Cre⁺ (Cxcl12^−/− EC) (Agarwal et al., 2019 (link)), Cxcl12^f/f-Prx1-Cre⁺ (Cxcl12^−/− MPC) (Agarwal et al., 2019 (link)), and Cxcl12^f/f-Ubc-Cre⁺ (Cxcl12^−/−) mice. Loss of CXCL12 expression in endothelial cells (Cxcl12^−/− EC) and mesenchymal progenitor cells (Cxcl12^−/− MPC) from these mice was previously confirmed by real time PCR (Agarwal et al., 2019 (link)). Global deletion of Cxcl12 in Cxcl12^f/f-Ubc-Cre⁺ mice was achieved by administration of 50 mg/kg of tamoxifen (Sigma-Aldrich; Cat no. T5648) in corn oil through intraperitoneal injections for five consecutive days. All mice were maintained in an AAALAC-accredited animal facility, and all procedures were carried out in accordance with federal guidelines and protocols approved by the Institutional Animal Care and Use Committee at the University of Alabama, Birmingham.