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

386 Citations (Scopus)

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
StatePublished - May 12 2000

Fingerprint

Cytochromes c
Apoptosis
Embryonic Structures
Cells
Cell Line
Mitochondria
Staurosporine
Oxidative Phosphorylation
Cell death
Caspase 3
DNA Damage
Cell Death
Chemical activation
Irradiation
DNA
Serum

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.

Cytochrome c deficiency causes embryonic lethality and attenuates stress-induced apoptosis. / Li, Kang; Li, Yucheng; Shelton, John M.; Richardson, James A.; Spencer, Erika; Chen, Zhijian J.; Wang, Xiaodong; Williams, R. Sanders.

In: Cell, Vol. 101, No. 4, 12.05.2000, p. 389-399.

Research output: Contribution to journalArticle

Li, K, Li, Y, Shelton, JM, Richardson, JA, Spencer, E, Chen, ZJ, Wang, X & Williams, RS 2000, 'Cytochrome c deficiency causes embryonic lethality and attenuates stress-induced apoptosis', Cell, vol. 101, no. 4, pp. 389-399.
Li, Kang ; Li, Yucheng ; Shelton, John M. ; Richardson, James A. ; Spencer, Erika ; Chen, Zhijian J. ; Wang, Xiaodong ; Williams, R. Sanders. / Cytochrome c deficiency causes embryonic lethality and attenuates stress-induced apoptosis. In: Cell. 2000 ; Vol. 101, No. 4. pp. 389-399.
@article{2b2803fe4cbe4d13a6f063ca386d66b8,
title = "Cytochrome c deficiency causes embryonic lethality and attenuates stress-induced apoptosis",
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.",
author = "Kang Li and Yucheng Li and Shelton, {John M.} and Richardson, {James A.} and Erika Spencer and Chen, {Zhijian J.} and Xiaodong Wang and Williams, {R. Sanders}",
year = "2000",
month = "5",
day = "12",
language = "English (US)",
volume = "101",
pages = "389--399",
journal = "Cell",
issn = "0092-8674",
publisher = "Cell Press",
number = "4",

}

TY - JOUR

T1 - Cytochrome c deficiency causes embryonic lethality and attenuates stress-induced apoptosis

AU - Li, Kang

AU - Li, Yucheng

AU - Shelton, John M.

AU - Richardson, James A.

AU - Spencer, Erika

AU - Chen, Zhijian J.

AU - Wang, Xiaodong

AU - Williams, R. Sanders

PY - 2000/5/12

Y1 - 2000/5/12

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=0034640102&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0034640102&partnerID=8YFLogxK

M3 - Article

VL - 101

SP - 389

EP - 399

JO - Cell

JF - Cell

SN - 0092-8674

IS - 4

ER -