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

C. Michael Knudson, Kenneth S K Tung, Warren G. Tourtellotte, Gary A J Brown, Stanley J. Korsmeyer*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

1270 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)96-99
Number of pages4
JournalScience
Volume270
Issue number5233
DOIs
StatePublished - 1995

ASJC Scopus subject areas

  • General

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