Kunio Yamazaki¹, G.K. Beauchamp¹, J. Bard², & E.A. Boyse²

We have shown that mice exhibit body odors of exquisite individuality (odortypes) representing polymorphism of Major Histocompatibility Complex (MHC) genes and less potently, of other chromosomal sites (reviewed by E.A. Boyse et al. 1991, in R. Ader, D.L. Felter and N. Cohen, eds., Psychoneuroimmunology-II, Academic Press, San Diego, pp831-846). Perception of odortype likely underlies mate selection, pregnancy success and parental behavior, serving to maintain normal social interactions and to promote genetic diversity through avoidance of inbreeding. Although several lines of evidence suggest MHC genes themselves code for odortypes, incontrovertible evidences of this would focus the search for mechanism directly on these known genes. Thus the purpose of this study was to determine whether mice with targeted gene disruptions (knock-out mice) that do not express one class of MHC genes (termed class I) differ in body odor from otherwise identical animals expressing these genes. Mice trained in a Y maze served as the bioassay. We tested the ability of 5 trained mice to distinguish the urine odor of C57BL/6J-₂m-deficient (-/-) male mice from the urine of control C57BL/6J (+/+) male mice. The results demonstrated that animals significantly distinguished (+/+) from (-/-) and generalized this response to distinguish (+/-) from (-/-). However, in generalization test they exhibited no tendency to discriminate the heterozygote (+/-) from the homozygote (+/+) suggesting class I effects are not quantitative. These data provide additional strong evidence that it is the MHC (class I) genes themselves that mediate MHC-determined differences in odortype.

Address:   Monell Chemical Senses Center 3500 Market Street Philadelphia PA 19104 USA, 215-898-3094, fax 215-898-2084, yamazaki@monell.org

¹Monell Chemical Senses Center, Philadelphia, PA 19104. ²University of Arizona, Tucson, AZ 85724.

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