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Inactivation of Insulin-Like Factor 6 Disrupts the Progression of Spermatogenesis at Late Meiotic Prophase

Institute of Human Genetics (O.B.-T., K.S., I.P., P.G., W.E., I.M.A.), University of Göttingen, D-37073 Göttingen, Germany; Department of Anatomy and Cell Biology (A.M.), University of Giessen, D-35385 Giessen, Germany; Department of Genetics and Evolution (P.G.), Institute of Zoology, University of Jagiellonian, PL-30060 Krakow, Poland

Address all correspondence and requests for reprints to: I. M. Adham, Institute of Human Genetics, University of Göttingen, D-37073 Göttingen, Germany. E-mail: iadham{at}gwdg.de.

Insulin-like factor 6 (INSL6), a member of the insulin-like superfamily, is predominantly expressed in male germ cells. Expression of the Insl6 is first detected in mouse testis at postnatal d 15 when the first wave of spermatogenesis progresses to pachytene spermatocytes. To elucidate the role of INSL6 in germ cell development, we generated Insl6-deficient mice. The majority of the Insl6-deficient males on a hybrid genetic background exhibited impaired fertility, whereas females were fertile. The number of mature sperm and sperm motility were drastically reduced in the epididymis. The reduced sperm count could be due to apoptotic death of a significant number of developing germ cells. Analysis of germ cell development during the juvenile life showed an arrest of the first wave of spermatogenesis in late meiotic prophase. RNA analysis revealed a significant decrease in expression of late meiotic- and postmeiotic-specific marker genes, whereas expression of early meiotic-specific genes remains unaffected in the Insl6^–/– testes. These results demonstrate that INSL6 is required for the progression of spermatogenesis.

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