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First published online August 20, 2008
doi: 10.1242/10.1242/jcs.032417

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Accelerated re-epithelialization in Dpr2-deficient mice is associated with enhanced response to TGFβ signaling

¹ Protein Sciences Laboratory of the Ministry of Education, Department of Biological Sciences and Biotechnology, Tsinghua University, Beijing 100084, People's Republic of China
² State Key Laboratory of Proteomics, Genetic Laboratory of Development and Diseases, Institute of Biotechnology, Beijing 100071, People's Republic of China

^* Authors for correspondence (e-mails: yangx{at}nic.bmi.ac.cn; mengam{at}mail.tsinghua.edu.cn)

Accepted 12 June 2008

Members of the Dapper (Dpr)/Dact protein family are involved in the regulation of distinct signaling pathways, including TGFβ/Nodal, canonical and noncanonical Wnt pathways. Three Dpr genes, Dpr1, Dpr2 and Dpr3, are expressed in mouse embryos and in many adult tissues; however, their in vivo functions have not been reported. In this study, we generated Dpr2-deficient mice using a gene-knockout approach. Homozygous Dpr2 knockout (Dpr2^–/–) embryos developed normally and postnatal Dpr2^–/– mice grew to adulthood without obvious morphological or behavioral defects. We found that Dpr2 was expressed highly in epidermal keratinocytes and in hair follicles of adult mice, and that Dpr2 deficiency resulted in accelerated re-epithelialization during cutaneous wound healing. Furthermore, we demonstrated that loss of Dpr2 function enhanced the responses of keratinocytes to TGFβ stimulation, and that TGFβ signals promoted adhesion to fibronectin and migration of keratinocytes, by regulating the expression of specific integrin genes. Thus, Dpr2 plays an inhibitory role in the re-epithelialization of adult skin wounds by attenuating TGFβ signaling.

Key words: Wound healing, Re-epithelialization, Keratinocyte, Dapper2, TGFβ