Open AccessApoptosis regulator Bcl-w is essential for spermatogenesis but appears otherwise redundant
Author(s) -
Cristin G. Print,
Kate L Loveland,
Leonie Gibson,
Terry Meehan,
Anna Stylianou,
Nigel G. Wreford,
David M de Kretser,
Donald Metcalf,
Frank Köntgen,
Jerry M. Adams,
Suzanne Cory
Publication year - 1998
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.95.21.12424
Subject(s) - spermatogenesis , biology , sertoli cell , apoptosis , sterility , andrology , sperm , homologous chromosome , haematopoiesis , gene , microbiology and biotechnology , germ cell , germline , embryo , genetics , stem cell , endocrinology , medicine
Proteins of the Bcl-2 family are important regulators of apoptosis in many tissues of the embryo and adult. The recently isolatedbcl-w gene encodes a pro-survival member of the Bcl-2 family, which is widely expressed. To explore its physiological role, we have inactivated thebcl-w gene in the mouse by homologous recombination. Mice that lack Bcl-w were viable, healthy, and normal in appearance. Most tissues exhibited typical histology, and hematopoiesis was unaffected, presumably due to redundant function with other pro-survival family members. Although female reproductive function was normal, the males were infertile. The testes developed normally, and the initial, prepubertal wave of spermatogenesis was largely unaffected. The seminiferous tubules of adult males, however, were disorganized, contained numerous apoptotic cells, and produced no mature sperm. Both Sertoli cells and germ cells of all types were reduced in number, the most mature germ cells being the most severely depleted. Thebcl-w −/− mouse provides a unique model of failed spermatogenesis in the adult that may be relevant to some cases of human male sterility.