The linkage of the major histocompatibility complex (MHC) and the growth and reproduction complex (Grc) in the rat was studied in an F2 hybrid population generated from female BIL/1 (RT1l-Grc) and male YO (RT1u-Grc+) animals: 1.722 offspring were born, and 1,568 were weaned and studied. The body weights of the offspring segregated with the RT1 haplotype of the MHC, and the RT1l homozygotes were significantly smaller than their RT1l/u and RT1u/u littermates. The growth rate of the RT1l/l animals was approximately the same as that of the BIL/1 animals, and both were significantly less than the growth rates of the RT1l/u, RT1u/u, and YO (RT1u) animals. The testes of the RT1l animals showed an arrest of spermatogenesis at the early pachytene stage of the primary spermatocytes, and they were approximately 1/10 as heavy as the testes of the RT1l/u and RT1u/u animals. The ovaries in females of all three haplotypes had the same weight, but there was a decrease in the number of ova released per cycle in the RT1 l/l animals. The major loss of the RT1l homozygotes, which caused distortion of the phenotypic ratios among the offspring, did not occur in utero but in the early postnatal period before weaning. There were 7/1568 recombinants between the MHC, using the RT1.A antigen as the marker, and the Grc, using small body size (dw-3) as the marker, and 1/1568 recombinant between the loci influencing body size (dw-3) and fertility (ft) of the Grc. These data gave the following map distances (95% confidence levels): RT1.A to dw-3, 0.45 (0.25-0.96) centimorgans and dw-3 to ft, 0.07 (0.04-0.40) centimorgans. A female recombinant was used develop an inbred line carrying the RT1.Al-Grc+ chromosome.

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