Programmed cell death in invertebrates

Current Opinion in Genetics and Development

Volumn 6, Issue 1, 1996, Pages 34-38

  Hengartner, Michael O ^a  

^a Howard Hughes Medical Institute Cold Spring Harbor Laboratory Cold Spring Harbor   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

APOPTOSIS; CAENORHABDITIS ELEGANS; CELL DEATH; CELL KILLING; CELL PROTECTION; DROSOPHILA MELANOGASTER; EVOLUTION; GENE ISOLATION; GENETIC ANALYSIS; INVERTEBRATE; NONHUMAN; PRIORITY JOURNAL; SHORT SURVEY;

CAENORHABDITIS ELEGANS; DROSOPHILA MELANOGASTER; INVERTEBRATA; MELANOGASTER;

EID: 0030050416     PISSN: 0959437X     EISSN: None     Source Type: Journal    
DOI: 10.1016/S0959-437X(96)90007-6     Document Type: Article

References (13)

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4. Ellis RE, Yuan J, Horvitz HR: Mechanisms and functions of cell death. Annu Rev Cell Biol 1991, 7:663-698.
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6. Ellis HM, Horvitz HR: Genetic control of programmed cell death in the nematode C. etegans Cell 1986, 44:817-829.
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8. Hengartner MO, Horvitz HR: The ins and outs of programmed cell death in C elegans. Phil Trans R Soc Lond [Biol] 1994, 345:243-246.
9. Hengartner MO, Horvitz HR: C. elegans cell death gene ced-9 encodes a functional homolog of mammalian proto-oncogene bcl-2. Cell 1994, 76:665-676. This paper describes the molecular characterization of C. elegans ced-9. It shows that CED-9 is a member of the Bcl-2 family and that Bcl-2 can partially rescue ced-9 mutants.
10. Vaux DL, Weissman IL, Kim SK: Prevention of programmed cell death in Caenorhabditis elegans by human bcl-2. Science 1992, 258:1955-1957.
11. Vaux DL, Haecker G, Strasser A: An evolutionary perspective on apoptosls. Cell 1994, 76:777-779.
12. Hengartner MO, Horvitz HR: Programmed cell death in C. elegans. Curr Opin Genet Dev 1994, 4:581-586.
13. Hengartner MO, Horvitz HR: Activation of C. elegans cell death protein CED-9 by an amino-acid substitution in a domain conserved in Bcl-2. Nature 1994, 369:318-320. This paper identifies a gain-of-function mutation in ced-9 as a missense mutation affecting a residue conserved in all Bcl-2 family members. It also suggests that ced-9 possesses both death-suppressing and death-promoting activities.