The testicular fatty acid binding protein PERF15 regulates the fate of germ cells in PERF15 transgenic mice

The quality control of sperm is critical for efficient reproduction. In germ cells, cell death involves different processes to those in somatic cells, and in many cases, the trigger to induce cell death in deficient germ cells is still unclear. It is known that the fatty acid composition of sperm is...

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Veröffentlicht in:Development, growth & differentiation growth & differentiation, 2005-01, Vol.47 (1), p.15-24
Hauptverfasser: Kido, Tatsuo, Arata, Satoru, Suzuki, Ryusuke, Hosono, Tomohiko, Nakanishi, Yoshinobu, Miyazaki, Jun‐ichi, Saito, Izumu, Kuroki, Toshio, Shioda, Seiji
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Sprache:eng
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Zusammenfassung:The quality control of sperm is critical for efficient reproduction. In germ cells, cell death involves different processes to those in somatic cells, and in many cases, the trigger to induce cell death in deficient germ cells is still unclear. It is known that the fatty acid composition of sperm is related to fertility. Composition of the fatty acid of germ cells changes dynamically during spermatogenesis, and fatty acid binding protein (FABP) may be involved in these changes. In this study, we developed transgenic mice with a testicular germ‐cell‐specific FABP (PERF15) transgene, whose expression was controlled by the Cre‐LoxP site‐specific recombination system. We also developed transgenic mice with the Cre gene under the control of the spermatocyte specific Pgk2 promoter. In double transgenic mice, following Cre‐mediated recombination of the PERF15 containing transgene, PERF15 was strongly overexpressed. Its overexpression induced multinucleate symplasts to form, indicating programmed germ cell death occurred at the elongated spermatid stage. As a result, sperm harboring the transgene were significantly decreased, but the surviving sperm demonstrated higher fertility than natural sperm. Therefore, we conclude that PERF15 associate with the direction of germ cell fates and preserve the quality of sperm.
ISSN:0012-1592
1440-169X
DOI:10.1111/j.1440-169x.2004.00775.x