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Testicular degeneration in Bclw-deficient mice.

TitleTesticular degeneration in Bclw-deficient mice.
Publication TypeJournal Article
Year of Publication1998
AuthorsRoss AJ, Waymire KG, Moss JE, Parlow AF, Skinner MK, Russell LD, MacGregor GR
JournalNat Genet
Volume18
Issue3
Pagination251-6
Date Published1998 Mar
ISSN1061-4036
KeywordsAge Factors, Amino Acid Sequence, Animals, Cloning, Molecular, Follicle Stimulating Hormone, Homozygote, Immunohistochemistry, Infertility, Male, Male, Mice, Mice, Inbred C57BL, Mice, Inbred Strains, Mice, Mutant Strains, Microscopy, Electron, Molecular Sequence Data, Proteins, Proviruses, Random Amplified Polymorphic DNA Technique, Sequence Analysis, Sertoli Cells, Spermatozoa, Testis, Tissue Distribution
Abstract

To identify genes required for mammalian spermatogenesis, we screened lines of mutant mice created using a retroviral gene-trap system for male infertility. Homozygous ROSA41 male mice exhibit sterility associated with progressive testicular degeneration. Germ-cell defects are first observed at 19 days post-natal (p19). Spermatogenesis is blocked during late spermiogenesis in young adults. Gradual depletion of all stages of germ cells results in a Sertoli-cell-only phenotype by approximately six months of age. Subsequently, almost all Sertoli cells are lost from the seminiferous tubules and the Leydig cell population is reduced. Molecular analysis indicates that the gene mutated is Bclw, a death-protecting member of the Bcl2 family. The mutant allele of Bclw in ROSA41 does not produce a Bclw polypeptide. Expression of Bclw in the testis appears to be restricted to elongating spermatids and Sertoli cells. Potential roles for Bclw in testicular function are discussed.

DOI10.1038/ng0398-251
Alternate JournalNat. Genet.
PubMed ID9500547
Grant List5 T32 GM08367 / GM / NIGMS NIH HHS / United States
HD-24875 / HD / NICHD NIH HHS / United States