Journal
EMBO JOURNAL
Volume 24, Issue 22, Pages 3963-3973Publisher
WILEY
DOI: 10.1038/sj.emboj.7600857
Keywords
apoptosis; BH3-only protein; Bik; Bim; spermatogenesis
Categories
Funding
- NCI NIH HHS [CA80188, R01 CA080188] Funding Source: Medline
Ask authors/readers for more resources
The BH3-only proteins of the Bcl-2 family initiate apoptosis through the activation of Bax-like relatives. Loss of individual BH3-only proteins can lead either to no phenotype, as in mice lacking Bik, or to marked cell excess, as in the hematopoietic compartment of animals lacking Bim. To investigate whether functional redundancy with Bim might obscure a significant role for Bik, we generated mice lacking both genes. The hematopoietic compartments of bik(-/-)bim(-/-) and bim(-/-) mice were indistinguishable. However, although testes develop normally in mice lacking either Bik or Bim, adult bik(-/-)bim(-/-) males were infertile, with reduced testicular cellularity and no spermatozoa. The testis of young bik(-/-)bim(-/-) males, like those lacking Bax, exhibited increased numbers of spermatogonia and spermatocytes, although loss of Bik plus Bim blocked spermatogenesis somewhat later than Bax deficiency. The initial excess of early germ cells suggests that spermatogenesis fails because supporting Sertoli cells are overwhelmed. Thus, Bik and Bim share, upstream of Bax, the role of eliminating supernumerary germ cells during the first wave of spermatogenesis, a process vital for normal testicular development.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available