The Journal of Heredity 2001:92(4)
© 2001 The American Genetic Association 92:322-326
Mapping of a QTL for Serum HDL Cholesterol in the Rabbit Using AFLP Technology
From the Department of Laboratory Animal Science, Faculty of Veterinary Medicine, Graduate School of Animal Health, Utrecht University, P.O. Box 80.166, NL-3508 TD Utrecht, The Netherlands (Van Haeringen, Bieman, Gillissen, Lankhorst, Van Zutphen, and Van Lith) and KeyGene N.V., Wageningen, The Netherlands (Kuiper). W. A. Van Haeringen is currently at the Dr. Van Haerigen Laboratorium B.V., Wageningen, The Netherlands, and M. T. R. Kuiper is currently at Aventis CropScience N.V., Gent, Belgium.
Address correspondence to H. A. Van Lith, Ph.D. at the address above or e-mail: lith{at}las.vet.uu.nl.
The amplified fragment length polymorphism (AFLP) technique is a DNA technology that generates the so-called AFLP markers. These markers are genomic restriction fragments detected after two rounds of polymerase chain reaction (PCR) without prior knowledge of nucleotide sequence. Here we describe the first application of the AFLP technique in the rabbit. We have tested two primer combinations. The results obtained with the DNA from rabbits of different breeds justify the conclusion that AFLP analysis is an effective tool for genetic studies in the rabbit. In addition, we contribute to the linkage map of the rabbit by localizing two AFLP markers on rabbit linkage group VI (LG VI). For this purpose the progeny of a IIIVO/JU x [IIIVO/JU x AX/JU1 backcross were genotyped for 12 AFLP markers and 3 LG VI classical markers [one coat color marker (e) and two biochemical markers (Es-1 and Est-2)]. AX/JU is a dietary cholesterol-susceptible (hyperresponding) inbred strain and IIIVO/JU is a dietary cholesterol resistant (hyporesponding) inbred strain. Moreover, it is possible to evoke dietary cholesterol-induced aorta atherosclerosis in a relatively short time period in AX/JU rabbits, in contrast to IIIVO/JU rabbits. A significant cosegregation was found between basal serum HDL cholesterol level (i.e., the level on a low-cholesterol, control diet) and an AFLP marker on LG VI. It is concluded that one or more genes of LG VI are regulating the basal serum HDL cholesterol level in rabbits. Thus the present study with rabbits clearly illustrates the value of AFLP markers for the construction of linkage maps and mapping of quantitative trait loci (QTL).
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