Poster Sessions

DEV-9

Joonsung Hwang

J. Hwang, R. Kita, J. Suh, M. Morasso

Role of Dlx3 in Hair Cycling

Ectodermal appendages such as hair and tooth are attractive models for understanding the mechanisms underlying epithelial-mesenchymal interactions. Dlx3 belongs to the Distal-less family of homeodomain transcription factors, and an autosomal dominant mutation in DLX3 is responsible for the ectodermal dysplasia termed Tricho-Dento-Osseous syndrome (TDO), characterized by defects in hair, tooth, and bone development. Recently, we assessed the function of Dlx3 as a crucial transcriptional regulator of hair formation and regeneration using a Cre-mediated knockout mouse model. The most striking defect in those mice was complete alopecia due to failure in hair morphogenesis and cycling. However, it is not clear that the failure of hair cycling is due to a direct result from Dlx3 loss or a secondary effect from an incomplete first anagen in the Cre-mediated knockout mouse. To further investigate the specific role of Dlx3 in the hair cycle, we are utilizing a tamoxifen-inducible system by crosses of K14-CreERT mice with Dlx3-floxed mice. Knockout of Dlx3 expression is accomplished by the topical application of tamoxifen during the first postnatal catagen, especially to avoid the cumulative effect from an incomplete hair cycle as mentioned above. Our preliminary results establish Dlx3 as an essential regulator of hair cycling, validated by the permanent hair loss in the inducible knockout mice.