Identification of wound healing/regeneration quantitative trait loci (QTL)at multiple time points that explain seventy percent of variance in (MRL/MpJ and SJL/J) mice F-2 population

Studies oil genetic mechanisms of wound healing in mammals are very few, al though injury is a leading cause of the global burden of disease. In this s tudy, we performed a high-density, genome-wide scan using 633 (MRL/MPJ x SJ L/J) F-2 intercross at multiple time points (days 15, 21, and 25) to identi fy quantitative trait loci (QTL) involved in Wound healing/regeneration. Th e hypothesis of the study was that QTL and unique epistatic interactions ar e involved at each time point to promote Wound healing/regeneration. Ten QT L were identified from chromosomes 1, 4, 6, 7, 9, and 13. Of the 10 QTL, ei ght from chromosomes 1, 4, 6, and 9 were novel as compared to QTL identifie d in the 1McBrearty et al. (1998) study. The 10 QTL altogether explained 70 % of variance in F-2 mice. The same QTL were identified at each time point, with simple linear correlation between days IS, 21, and 25, showing very h igh significant relationships (R >0.92, P <0.0001). Unique epistatic intera ctions were identified at each time point except those from chromosomes 4, 6, 9, and 13 that were found at all three time points, showing that some lo ci are involved at all the three time points of wound healing (days 15, 21, and 25). Therefore, loci-to-loci interactions may play a major role in wou nd healing. Information from these Studies may help in the identification o f genes that could be involved in wound healing/regeneration.