The morphologic features of the testicular defect in the rat caused by the genes of the growth and reproduction complex (grc), which are linked to the major histocompatibility complex (MHC), were examined by transmission and scanning electron microscopy in animals homozygous for grc (grc/grc), heterozygous for grc (grc/+), and normal (+/+). The testes of the grc homozygotes were small, and their tubular epithelium showed a loss of the normal organization. There were no sperm because the spermatogonia developed only to the pachytene stage of the primary spermatocyte; there was cellular degeneration and necrosis; and the basal lamina showed reduplication and invagination into the tubule. The number of the Sertoli cells was increased, their nuclei were displaced into the adluminal layers of the tubular epithelium, and their cytoplasm extended into the lumens. There was an increase in interstitial fibrous tissue, and the blood vessels deep in the parenchyma had thickened walls. In the heterozygotes, there was some architectural disorganization of the tubular epithelium and a greater number of tubules with a low concentration of sperm tails. Some of the intermediate spermatogonia were not attached to the basal lamina, and there was an increase in developmental abnormalities and abnormal sperm. The number of Sertoli cells was increased, and their nuclei extended into the second and third layers of the tubular epithelium. The homozygous wild type animals showed normal testicular development and normal spermatogenesis. This is the first description of a developmental defect in the rat that is under the control of a well-defined genetic system. It also is the first evidence for the morphologic expression of a heterozygous recessive gene in an animal that is phenotypically normal.