Keratinocyte Laboratory, Cancer Research UK London Research Institute, London, UK

Correspondence: Fiona M. Watt, Keratinocyte Laboratory, Cancer Research UK London Research Institute, 44 Lincoln's Inn Fields, London WC2A 3PX, UK. Email: fiona.watt@cancer.org.uk

Received 28 December 2004; Revised 25 July 2005; Accepted 29 July 2005; Published online 15 November 2005.

Abstract

There are conflicting reports of the consequences of deleting 1 integrins from the epidermis of transgenic mice. Epidermal thinning with normal differentiation and lack of inflammation has been observed; conversely, epidermal thickening, abnormal differentiation, and dermal fibrosis can occur. 1 integrin deletion results in decreased epidermal proliferation, yet on wounding the proliferative defect is overcome. To distinguish primary from secondary consequences of 1 integrin loss, we compared epidermal 1 deletion at E14.5 via K5Cre and 4-hydroxy-tamoxifen induced deletion in adulthood via K14CreER. As reported previously, there was dermo-epidermal splitting, inflammation, reduced proliferation, and hair follicle and sebaceous gland loss in 30-d-old K5Cre 1-null mice. These changes were not observed 30 d after 1 integrin deletion in adult epidermis, however, and there were no changes in the hair follicle stem cell compartment. Deletion in adult epidermis revealed a previously unreported correlation between the level of 1 integrins and proliferation in the interfollicular epidermis that was remarkably consistent with human epidermis. In addition, the number of melanocytes in interfollicular epidermis was greatly increased. Our results highlight the context-dependent effects of 1 integrin deletion and suggest that inflammation may be responsible for some of the K5Cre 1-null phenotype.