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2L, compare to H). However, in the area of the fully differentiated secretory ameloblasts, cells detached from the SI ( Fig. 2M, compare to I). These data showed that E-cadherin is essential for maintaining the integrity of cells in the laCLs. Next, we investigated whether E-cadherin affects cell proliferation and migration in the mouse incisor. We first analyzed whether loss of E-cadherin affected stem cell maintenance by counting LRC number. GliCreERT2;Cdh1fl/?;K5tTA;H2B-GFP mice were chased CPI-1205 with doxycycline to produce LRCs and injected with tamoxifen to delete Cdh1, and cells that were brightly GFP positive were counted (dimly positive cells were considered to be undergoing division). Deletion of E-cadherin significantly decreased the number of LRCs in the laCLs ( Fig. 3A�CC, pDEF6 in the laCL after E-cadherin deletion by staining for proliferating cell nuclear antigen (PCNA) and found that, in the mutants, PCNA positive cells were significantly increased compared to controls (Fig. 4A�CC, pMK-4827 mouse that cells migrated along the proximo-distal axis of the tooth. Adult mice were given a single intraperitoneal injection of BrdU to label dental epithelial cells during S-phase (n=3 mice per time point). The mice were then sacrificed 1.5, 24 or 48?h after injecting BrdU to visualize the distance that labeled cells had migrated from the laCL at these different time points. In controls, cells migrated out of the laCL towards the ameloblast region at a rate of approximately 470?��m per 24?h ( Fig. 5A�CC). This rate was slightly slower than that in rat and was similar to what was previously found in mouse with tritiated thymidine labeling, in which the migration rate was 408?��m per day ( Hwang and Tonna, 1965?and?Smith and Warshawsky, 1975).