Abstract
Congenic breeding strategies are becoming increasingly important as a greater number of complex trait linkages are identified. Traditionally, the development of a congenic strain has been a time-consuming endeavour, requiring ten generations of backcrosses. The recent advent of a dense molecular genetic map of the mouse permits methods that can reduce the time needed for congenic-strain production by 18–24 months. We present a theoretical evaluation of marker-assisted congenic production and provide the empirical data that support it. We present this ‘speed congenic’ method in a user-friendly manner to encourage other investigators to pursue this or similar methods of congenic production.
References
Markel, P.M., Bennett, B., Beeson, M., Gordon, L. & Johnson, I.E. Confirmation of quantitative trait loci for ethanol sensitivity. Genome Res. 7, 92–99 (1997).
Oettgen, H.C. et al. Active anaphylaxis in IgE-deficient mice. Nature 370, 367–370 (1994).
Ghosh, S. et al. Polygenic control of autoimmune diabetes in nonobese diabetic mice. Nature Genet. 4, 404–409 (1993).
Taylor, B.A. & Phillips, S.J. Detection of obesity QTLs on mouse chromosomes 1 and 7 by selective DNA pooling. Genomics 34, 389–398 (1996).
York, B., Lei, K. & West, D.B. Sensitivity to dietary obesity linked to a locus on chromosome 15 in a CAST/Ei×C57BL/6J intercross. Mamm. Genome 7, 677–681 (1996).
Yui, M.A. et al. Production of congenic mouse strains carrying NOD-derived diabetogenic genetic intervals: an approach for the genetic dissection of complex traits. Mamm. Genome 7, 331–334 (1996).
Morel, L., Yu, Y., Blenman, K.R., Caldwell, R.A. & Wakeland, E.K. Production of congenic mouse strains carrying genomic intervals containing SLE-susceptability genes derived from SLE-prone NZM2410. Mamm. Genome 7, 335–339 (1996).
Green, E.L., ed. Biology of the Laboratory Mouse (McGraw-Hill, New York, 1966).
Silver, L., Concepts and Applications (Oxford University Press, New York, 1995).
Plump, A.S. et al. Severe hypercholesterolemia and atherosclerosis in apolipoprotein E-deficient mice created by homologous recombination in ES cells. Cell 71, 343–353 (1992).
Paigen, B., Morrow, A., Brandon, C., Mitchell, D. & Holmes, P. Variation in susceptibility to atherosclerosis among inbred strains of mice. Atherosclerosis 57, 65–73 (1985).
Zhang, S., Reddick, R.L., Piedrahita, J.A. & Maeda, N. Spontaneous hypercholesterolemia and arterial lesions in mice lacking apolipoprotein E. Science 258, 468–471 (1992).
Threadgill, D.W. et al. SSLPsto map genetic differences between the 129 strains and closed-colony, random-bred CD-1 mice. Mamm. Genome 8, 441–442 (1997).
Simpson, E.M. et al. Genetic variation among 129 substrains and its importance for targeted mutagenesis in mice. Nature Genet. 16, 19–27 (1997).
Kleynr, P.W. et al. Identification and characterization of the mouse obesity gene tubby: a member of a novel gene family. Cell 85, 281–290 (1996).
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Markel, P., Shu, P., Ebeling, C. et al. Theoretical and empirical issues for marker-assisted breeding of congenic mouse strains. Nat Genet 17, 280–284 (1997). https://doi.org/10.1038/ng1197-280
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DOI: https://doi.org/10.1038/ng1197-280
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