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 TNFalpha. These results define the role of cytochrome c in different apoptotic signaling cascades.
authors.affiliation: Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas 75390, USA.
authors.forename: K
authors.initials: K
authors.lastname: Li
authors.forename: Y
authors.initials: Y
authors.lastname: Li
authors.forename: J M
authors.initials: JM
authors.lastname: Shelton
authors.forename: J A
authors.initials: JA
authors.lastname: Richardson
authors.forename: E
authors.initials: E
authors.lastname: Spencer
authors.forename: Z J
authors.initials: ZJ
authors.lastname: Chen
authors.forename: X
authors.initials: X
authors.lastname: Wang
authors.forename: R S
authors.initials: RS
authors.lastname: Williams
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D003574:Cytochrome c Group / Q000172:deficiency* / Q000235:genetics; D020964:Embryo Loss; D004622:Embryo, Mammalian / Q000378:metabolism* / Q000473:pathology*; D005314:Embryonic and Fetal Development / Q000502:physiology; D018507:Gene Expression Regulation, Developmental; D051379:Mice
chemical_list: D003574:Cytochrome c Group