Quantitative trait loci for compensatory renal hypertrophy in the mouse.
Reduction in numbers of nephrons or decrease in kidney function due to a variety of diseases results in compensatory renal hypertrophy (CRH). Recently, it has been proposed that CRH may be a prerequisite for progression of renal injury; genetic dissection of CRH may be therefore helpful in understanding the process whereby people with partial renal insufficiency progress to end-stage renal disease. Since genetic analysis of CRH in humans is quite limited, we searched for genetic determinants of CRH after unilateral nephrectomy using a total genome scan of the mouse BXD recombinant inbred strains. We demonstrated that CRH is a highly heritable trait and we identified a quantitative trait locus on mouse chromosome 11 near the D11Mit14 marker that exerts a major effect on CRH (lod score = 3.4) and is responsible for approximately 52% of genetic variation in CRH. This marker maps near Ace, Gh, and Ngfr positional candidate genes.
Institute of Physiology, Czech Academy of Sciences, Prague, Czech Republic.
V
V
Zídek
A
A
Musilová
J
J
Vorlíèek
M
M
Simáková
M
M
Pravenec
D000818:Animals; D002874:Chromosome Mapping; D006984:Hypertrophy; D007668:Kidney / Q000033:anatomy & histology / Q000473:pathology*; D007674:Kidney Diseases / Q000235:genetics* / Q000473:pathology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008811:Mice, Inbred DBA; D008817:Mice, Mutant Strains; D009929:Organ Size; D019655:Quantitative Trait, Heritable; D011995:Recombination, Genetic