The B1 strain of rats carries a unique mutation which causes defects in growth and reproduction: the males and females are small, the testes are hypoplastic and aspermatic, and the females have a reduced reproductive capacity. The loci controlling these defects are linked to the major histocompatibility complex (MHC) as determined by segregation studies in backcross and F2 hybrid populations. The levels of pituitary hormones and somatomedin C in the B1 strain are elevated or normal, and the testosterone level is elevated relative to the size of the testes. These findings suggest that hormone deficiencies are not the cause of these defects. The genes governing these defects have been designated the growth and reproduction complex (Grc). The recessive gene regulating small body size has been designated dw-3 (dwarf-3), and the recessive gene influencing reproductive capacity has been designated f. The Grc and MHC are separable by recombination, and the dw-3 and f genes are also separable by recombination. Studies in the (B1 X DA)F2 hybrid indicate that the map distance between the Grc and the MHC is 0.6 cM. Segregation distortion due to a deficiency of RT11 homozygotes is seen in some F2 hybrid populations derived from the B1 strain. Litter size data suggest that the loss of the RT11 homozygotes is due to intrauterine death. There is no apparent sex influence on the inheritance of the Grc, at least as it is presently understood, since it can be transmitted by either females or males. The growth and reproduction complex in the rat may be the analog of the T/t complex in the mouse, and the importance of the region of the chromosome adjacent to the major histocompatibility complex in the control of developmental processes may be a general phenomenon in mammals.