期刊名称：Proceedings of the National Academy of Sciences
印刷版ISSN：0027-8424
电子版ISSN：1091-6490
出版年度：1998
卷号：95
期号：20
页码：11792-11797
DOI：10.1073/pnas.95.20.11792
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：Wound healing of mammalian tissue is an essential process in the maintenance of body integrity. The general mechanism of wound healing usually studied in adult mammals is repair, in contrast to the regeneration seen in more primitive vertebrates. We recently have discovered that MRL/MpJ mice, unlike all other strains of mice tested, undergo rapid and complete wound closure that resembles regeneration. Specifically, through-and-through surgical ear hole wounds close without scarring in <4 weeks with normal gross and microanatomic architecture, including chondrogenesis. We also demonstrated that this healing is a heritable trait in inbred mice. In this study, we present results pertaining to its genetic control in progeny segregating for this phenotype. To identify the genetic loci that control the wound closure process, a genome-wide scan was performed on (MRL/MpJ-Faslpr x C57BL/6)F2 and backcross populations. In the primary screens of these populations, quantitative trait loci that control the extent of wound closure were detected on chromosomes 8, 12, and 15 and at two separate locations on chromosome 13. Evidence of further genetic control of healing was found on chromosome 7. All alleles that contribute to full wound closure are derived from the MRL/MpJ-Faslpr parent except for the quantitative trait locus on chromosome 8, which is derived from C57BL/6.
