Cytochrome c deficiency causes embryonic lethality and attenuates stress-induced apoptosis

Kang Li, Yucheng Li, John M. Shelton, James A. Richardson, Erika Spencer, Zhijian J. Chen, Xiaodong Wang, R. Sanders Williams

Research output: Contribution to journalArticle

394 Scopus citations

Abstract

Cytochrome c released from mitochondria has been proposed to be an essential component of an apoptotic pathway responsive to DNA damage and other forms of cell stress. Murine embryos devoid of cytochrome c die in utero by midgestation, but cell lines established from early cytochrome c null embryos are viable under conditions that compensate for defective oxidative phosphorylation. As compared to cell lines established from wild-type embryos, cells lacking cytochrome c show reduced caspase-3 activation and are resistant to the proapoptotic effects of UV irradiation, serum withdrawal, or staurosporine. In contrast, cells lacking cytochrome c demonstrate increased sensitivity to cell death signals triggered by TNFα. These results define the role of cytochrome c in different apoptotic signaling cascades.

Original languageEnglish (US)
Pages (from-to)389-399
Number of pages11
JournalCell
Volume101
Issue number4
Publication statusPublished - May 12 2000

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ASJC Scopus subject areas

  • Cell Biology
  • Molecular Biology

Cite this

Li, K., Li, Y., Shelton, J. M., Richardson, J. A., Spencer, E., Chen, Z. J., ... Williams, R. S. (2000). Cytochrome c deficiency causes embryonic lethality and attenuates stress-induced apoptosis. Cell, 101(4), 389-399.