1. ¹Molecular Genetics Division, Musculoskeletal Disease Center, JL Pettis VA Medical Center and Loma Linda University, Loma Linda, CA 92357, USA
2. ²Department of Botany and Plant Sciences, University of California, Riverside, CA 92521-0124, USA

Correspondence: David J Baylink, Musculoskeletal Disease Center, JL Pettis VA Medical Center, 11201 Benton Street (151), Loma Linda, CA 92357, USA E-mail: baylid@lom.med.va.gov

Received 8 August 2000; Accepted 8 February 2001.

Abstract

There have been few studies of the inheritance of wound healing in mammals. In this study, we demonstrate that inbred strains of mice differ significantly in the rate of wound healing. Of the 20 strains tested, fast healers (MRL/MpJ-Fas^lpr and LG/J) healed wounds four times faster than slow healers (Balb/cByJ and SJL/J). The genetic basis underlying the difference in the healing capacity was analysed using F₂ populations of two different crosses. We show that the wound healing is a polygenically determined quantitative trait with an average estimated heritability of 86%. The modes of gene action in these two crosses are different. In the (MRL/MpJ SJL/J) cross, genes regulating fast healing in MRL/MpJ mice exhibited additive effects, whereas these effects were suppressed by a dominant repressor gene in CBA/J mice in the (MRL/MpJ-Fas^lpr CBA/J) cross. Information gained from this investigation provides insight into further study of molecular mechanisms underlying the rate of wound healing in mammals.