Document Detail

Somatic gonad sheath cells and Eph receptor signaling promote germ-cell death in C. elegans.
MedLine Citation:
PMID:  22240896     Owner:  NLM     Status:  MEDLINE    
Programmed cell death eliminates unwanted cells during normal development and physiological homeostasis. While cell interactions can influence apoptosis as they do other types of cell fate, outside of the adaptive immune system little is known about the intercellular cues that actively promote cell death in healthy cells. We used the Caenorhabditis elegans germline as a model to investigate the extrinsic regulators of physiological apoptosis. Using genetic and cell biological methods, we show that somatic gonad sheath cells, which also act as phagocytes of dying germ cells, promote death in the C. elegans germline through VAB-1/Eph receptor signaling. We report that the germline apoptosis function of VAB-1 impacts specific cell death pathways, and may act in parallel to extracellular signal-regulated kinase MAPK signaling. This work defines a non-autonomous, pro-apoptotic signaling for efficient physiological cell death, and highlights the dynamic nature of intercellular communication between dying cells and the phagocytes that remove them.
X Li; R W Johnson; D Park; I Chin-Sang; H M Chamberlin
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, Non-P.H.S.     Date:  2012-01-13
Journal Detail:
Title:  Cell death and differentiation     Volume:  19     ISSN:  1476-5403     ISO Abbreviation:  Cell Death Differ.     Publication Date:  2012 Jun 
Date Detail:
Created Date:  2012-05-07     Completed Date:  2012-09-10     Revised Date:  2013-06-26    
Medline Journal Info:
Nlm Unique ID:  9437445     Medline TA:  Cell Death Differ     Country:  England    
Other Details:
Languages:  eng     Pagination:  1080-9     Citation Subset:  IM    
Department of Molecular Genetics, The Ohio State University, Columbus, OH 43210, USA.
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MeSH Terms
Caenorhabditis elegans / metabolism
Caenorhabditis elegans Proteins / antagonists & inhibitors,  genetics,  metabolism*
Cell Cycle Proteins / antagonists & inhibitors,  genetics,  metabolism*
Germ Cells / cytology,  metabolism
Gonads / cytology,  metabolism*
Mitogen-Activated Protein Kinase Kinases / metabolism
RNA Interference
Receptor Protein-Tyrosine Kinases / antagonists & inhibitors,  genetics,  metabolism*
Signal Transduction
Reg. No./Substance:
0/Caenorhabditis elegans Proteins; 0/Cell Cycle Proteins; EC Protein-Tyrosine Kinases; EC protein, C elegans; EC Protein Kinase Kinases

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

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