Defects in regulation of apoptosis in caspase-2-deficient mice

Louise Bergeron, Gloria I. Perez, Glen Macdonald, Lianfa Shi, Yi Sun, Andrea Jurisicova, Sue Varmuza, Keith E. Latham, Jodi A. Flaws, Jessica C.M. Salter, Hideaki Hara, Michael A. Moskowitz, En Li, Arnold Greenberg, Jonathan L. Tilly, Junying Yuan

Research output: Contribution to journalArticlepeer-review


During embryonic development, a large number of cells die naturally to shape the new organism. Members of the caspase family of proteases are essential intracellular death effectors. Herein, we generated caspase-2- deficient mice to evaluate the requirement for this enzyme in various paradigms of apoptosis. Excess numbers of germ cells were endowed in ovaries of mutant mice and the oocytes were found to be resistant to cell death following exposure to chemotherapeutic drugs. Apoptosis mediated by granzyme B and perforin was defective in caspase-2-deficient B lymphoblasts. In contrast, cell death of motor neurons during development was accelerated in caspase-2-deficient mice. In addition, caspase-2-deficient sympathetic neurons underwent apoptosis more effectively than wild-type neurons when deprived of NGF. Thus, caspase-2 acts both as a positive and negative cell death effector, depending upon cell lineage and stage of development.

Original languageEnglish (US)
Pages (from-to)1304-1314
Number of pages11
JournalGenes and Development
Issue number9
StatePublished - May 1 1998
Externally publishedYes


  • Apoptosis
  • Caspase-2
  • Caspases
  • Cell death
  • Ich1
  • Nedd2

ASJC Scopus subject areas

  • Genetics
  • Developmental Biology


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