Reduced Fertility in Female Homozygotes for <i>hgn</i> (Male Hypogonadism) Selected by <i>hgn</i>‐Associated Hypoplastic Kidney

Abstract

Abstract The male hypogonadism rat ( hgn/hgn ) shows a characteristic male sterility as a single autosomal recessive trait. Recently, the female homozygotes for hgn , assumed to be fertile, could be detected by a /jgji‐associated hypoplastic kidney ( hpk/hpk ). The present study was to investigate a possible influence of the hgn gene on female reproduction. The hgn/hgn females showed a significant growth retardation as compared with the phenotypically normal ones ( +/? ; +/hgn or +/+ ). The litter size at birth and number of implantation traces were significantly less in the hgn/hgn than in the +/? females. The hgn/hgn females became anestrous and infertile much earlier than the +/? did. Histologically, there were a few corpora lutea, some atretic follicles at different stages of maturation and abundant abnormal interstitial cells with pyknotic or karyorexic nuclei in the ovaries of hgn/hgn females that have been infertile. The birth rate expressed by per cent litter size at birth against number of implantation traces was comparable between the hgn/hgn and the +/? female, suggesting that the small litter size of hgn/hgn female could not be due to the embryonic death in utero. Nevertheless, the number of the tubal ova at estrous was comparable in the hgn/hgn and +/? females. Therefore, it was suggested that the half of ova or embryos may be lost during the period from the fertilization to the implantation. Histological appearances of the neonatal ovary in the hgn/hgn seemed hypoplastic. The number of cells including oocytes and interstitial cells, enzymatically separated from neonatal ovary, was significantly less in the hgn/hgn than in the +/hgn. These results suggest that the gene product(s) coded by normal allele of hgn gene(s) involves normal gonadal development in both sexes; the defect may lead testicular dysmorphology in the male and reduced fertility in the female.