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Bax-deficient mice with lymphoid hyperplasia and male germ cell death.

BAX, a heterodimeric partner of BCL2, counters BCL2 and promotes apoptosis in gain-of-function experiments. A Bax knockout mouse was generated that proved viable but displayed lineage-specific aberrations in cell death. Thymocytes and B cells in this mouse displayed hyperplasia, and Bax-deficient ovaries contained unusual atretic follicles with excess granulosa cells. In contrast, Bax-deficient males were infertile as a result of disordered seminiferous tubules with an accumulation of atypical premeiotic germ cells, but no mature haploid sperm. Multinucleated giant cells and dysplastic cells accompanied massive cell death. Thus, the loss of Bax results in hyperplasia or hypoplasia, depending on the cellular context.

Pubmed ID: 7569956


  • Knudson CM
  • Tung KS
  • Tourtellotte WG
  • Brown GA
  • Korsmeyer SJ


Science (New York, N.Y.)

Publication Data

October 6, 1995

Associated Grants

  • Agency: NCI NIH HHS, Id: CA49712
  • Agency: NICHD NIH HHS, Id: HD27500
  • Agency: NICHD NIH HHS, Id: P30-HD28934

Mesh Terms

  • Animals
  • Apoptosis
  • B-Lymphocytes
  • Female
  • Granulosa Cells
  • Hyperplasia
  • Infertility, Male
  • Lymphoid Tissue
  • Male
  • Mice
  • Mice, Knockout
  • Ovary
  • Proto-Oncogene Proteins
  • Proto-Oncogene Proteins c-bcl-2
  • Seminiferous Tubules
  • Spermatids
  • Spermatocytes
  • Spermatogenesis
  • Spermatozoa
  • T-Lymphocytes
  • bcl-2-Associated X Protein