Maintenance of spermatogenesis requires TAF4b, a gonad-specific subunit of TFIID

  1. Allison E. Falender1,
  2. Richard N. Freiman3,
  3. Kenneth G. Geles4,
  4. Kirk C. Lo2,5,
  5. KeumSil Hwang6,
  6. Dolores J. Lamb1,2,
  7. Patricia L. Morris6,
  8. Robert Tjian4, and
  9. JoAnne S. Richards1,7
  1. 1Department of Molecular and Cellular Biology, 2Scott Department of Urology, Baylor College of Medicine, Houston, Texas 77030, USA; 3Department of Molecular and Cell Biology and Biochemistry, Brown University, Providence, Rhode Island 02921, USA; 4Howard Hughes Medical Institute, Department of Molecular and Cell Biology, University of California at Berkeley, Berkeley, California 94720, USA; 5Mount Sinai Hospital, Division of Urology, University of Toronto, Toronto, Ontario, Canada M5G 1X5; 6Population Council, The Rockefeller University, New York, New York 10021, USA

Abstract

The establishment and maintenance of spermatogenesis in mammals requires specialized networks of gene expression programs in the testis. The gonad-specific TAF4b component of TFIID (formerly TAFII105) is a transcriptional regulator enriched in the mouse testis. Herein we show that TAF4b is required for maintenance of spermatogenesis in the mouse. While young Taf4b-null males are initially fertile, Taf4b-null males become infertile by 3 mo of age and eventually exhibit seminiferous tubules devoid of germ cells. At birth, testes of Taf4b-null males appear histologically normal; however, at post-natal day 3 gonocyte proliferation is impaired and expression of spermatogonial stem cell markers c-Ret, Plzf, and Stra8 is reduced. Together, these data indicate that TAF4b is required for the precise expression of gene products essential for germ cell proliferation and suggest that TAF4b may be required for the regulation of spermatogonial stem cell specification and proliferation that is obligatory for normal spermatogenic maintenance in the adult.

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Footnotes

  • Supplemental material is available at http://www.genesdev.org.

  • Article published online ahead of print. Article and publication date are at http://www.genesdev.org/cgi/doi/10.1101/gad.1290105.

  • ↵7 Corresponding author.

    ↵7 E-MAIL joanner{at}bcm.tmc.edu; FAX (713) 790-1275.

    • Accepted February 17, 2005.
    • Received December 15, 2004.
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  1. Published in Advance March 17, 2005, doi: 10.1101/gad.1290105 Genes & Dev. 19: 794-803 Cold Spring Harbor Laboratory Press

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