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Type II Gonadotropin-Releasing Hormone Receptor Transcripts in Human Sperm¹

^a Department of Biochemistry, University of Stellenbosch, Matieland, Stellenbosch 7602, Republic of South Africa ^b Center for Molecular Medicine and Genetics, ^c Department of Obstetrics and Gynecology, Institute for Scientific Computing, Wayne State University School of Medicine, Detroit, Michigan 48201

GnRH regulates reproduction via the well-characterized mammalian pituitary GnRH receptor (type I). In addition, two homologous genes for a second form of the GnRH receptor (type II) are present in the human genome, one on chromosome 14 and the second on chromosome 1. The chromosome 14 gene is ubiquitously transcribed at high levels in the antisense orientation but lacks exon 1, required to encode a full-length receptor. In comparison, the chromosome 1 gene contains all three exons. The issue of whether this gene is transcribed in any human tissue(s), and whether these transcripts encode a functional receptor protein, remains unresolved. We have directly addressed this by screening a panel of human RNAs by hybridization and RT-PCR. These analyses showed that, unlike the chromosome 14 gene, chromosome 1 gene expression is limited and of low abundance. Exon 1-containing transcripts were detected by in situ hybridization in mature sperm and in human postmeiotic testicular cells. Further sequence analysis revealed that although all the potential coding segments were present, the human transcripts, like the gene, contain a stop codon within the coding region and a frame-shift relative to other mammalian GnRH receptors. Although this suggests that the human gene may be a transcribed pseudogene, a functional type II GnRH receptor cDNA has recently been cloned from monkeys. Given the well-established role of GnRH in spermatogenesis and reported evidence of type II GnRH receptor immunoreactivity in human tissues, it is possible that the chromosome 1 gene is functional.

¹ Supported by grant 2047247 from the National Research Foundation of South Africa and a grant from the South African Medical Research Council to J.H., and in part by NIH grant HD36512 to S.A.K. S.W. is supported in part by a WSU GRE fellowship.

² Correspondence: J. Hapgood, Department of Biochemistry, University of Stellenbosch, Private Bag X1, Matieland, Stellenbosch 7602, Republic of South Africa. FAX: 2721 808 5863; jhap{at}sun.ac.za

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