Document Detail

Programmed cell death in the nematode C. elegans.
MedLine Citation:
PMID:  10548877     Owner:  NLM     Status:  MEDLINE    
Programmed cell death is a common feature during animal development. In the nematode C. elegans, more than 12 genes have been identified that function in the apoptotic killing and elimination of 131 of the 1090 cells that are generated during hermaphrodite development. These genes divide the process of programmed cell death into three distinct steps: execution of the death sentence; engulfment of dying cells; and degradation of dead, engulfed cells. Biochemical characterization of the genes in this pathway has led to the identification of an apoptotic machinery that mediates apoptotic death in this species. The proximal cause of apoptosis in C. elegans is the activation of the caspase homolog CED-3 from the inactive zymogen (proCED-3) into the mature protease. This activation is mediated by the Apaf-1 homolog CED-4. In cells that should survive, CED-3 and CED-4 pro-apoptotic activity is antagonized by the Bcl-2 family member CED-9. CED-9 has been proposed to prevent death by sequestering CED-4 and proCED-3 in an inactive ternary complex, the apoptosome. In cells fated to die, CED-9 is, in turn, inactivated by the pro-apoptotic BH3 domain-containing protein EGL-1, likely through a direct protein-protein interaction. The structural and functional conservation of cell death genes between nematodes and mammals strongly suggests that the apoptotic program is ancient in origin and that all metazoans share a common mechanism of apoptotic cell killing.
M O Hengartner
Related Documents :
11006337 - Jasmonic acid signaling modulates ozone-induced hypersensitive cell death.
19293697 - Isoflurane inhibits growth but does not cause cell death in hippocampal neural precurso...
7661027 - The measurement of deoxynucleotide (dntp) pools by radioimmunoassay (ria).
21534877 - Bone marrow stromal cells protect myeloma cells from bortezomib induced apoptosis by su...
8752677 - Expression of e and p-cadherin by melanoma cells decreases in progressive melanomas and...
1705757 - Carbonic anhydrase and proton secretion in turtle bladder mitochondrial-rich cells.
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review    
Journal Detail:
Title:  Recent progress in hormone research     Volume:  54     ISSN:  0079-9963     ISO Abbreviation:  Recent Prog. Horm. Res.     Publication Date:  1999  
Date Detail:
Created Date:  1999-12-08     Completed Date:  1999-12-08     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0404471     Medline TA:  Recent Prog Horm Res     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  213-22; discussion 222-4     Citation Subset:  IM    
Cold Spring Harbor Laboratory, New York 11724, USA.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Apoptosis / physiology
Caenorhabditis elegans / anatomy & histology*
Mammals / anatomy & histology
Grant Support

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

Previous Document:  Phytoestrogens in health and disease.
Next Document:  Control of apoptosis signaling by Apo2 ligand.