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. 2012 Feb 13;109(9):3463–3468. doi: 10.1073/pnas.1118823109

Fig. 1.

Fig. 1.

cTEC specific cytoablation. (A) Schematic representation of the Ccx-ckr1:DTR transgene. (B) Flow cytometric isolation of stromal components. Neural-crest derived mesenchymal cells (MEC), EpCam−, CD45−, CD31−, Ly51+ marker (Center); endothelial cells (EC), EpCam−CD45−CD31+Ly51− (Center); cTECs, EpCam+CD45−Ly51+UEA-1− (Right); and mTECs, EpCam+CD45−Ly51−UEA1+ (Right). (C) Expression levels of the endogenous Ccx-ckr1 gene, the Ccx-ckr1:eGFP knock-in allele, and the Ccx-ckr1:hDTR transgene in Ccx-ckr1eGFP/+ control (ctrl) and Ccx-ckr1eGFP/+;Ccx-ckr1:DTR transgenic (tg) mice. Results of quantitative RT-PCR normalized to the expression levels of Hprt are expressed relative to the levels of Ccx-ckr1:hDTR transgenic cTECs (dashed line). (D) Absolute numbers of TEC subsets (Left) and MECs and ECs (Right) of untreated and diphtheria toxin (DT)-treated nontransgenic (ctrl) or hDTR-transgenic mice (tg); animals received a single injection of DT (30 ng/g body weight, i.p.) and were analyzed 1 d (P8) thereafter. Statistical analysis was performed using Fisher´s t test (***P < 0.001).