Two C. elegans genes control the programmed deaths of specific cells in the pharynx

Development ◽  
1991 ◽  
Vol 112 (2) ◽  
pp. 591-603 ◽  
Author(s):  
R.E. Ellis ◽  
H.R. Horvitz

The genes ces-1 and ces-2 control the decisions of two cells in the nematode Caenorhabditis elegans to undergo programmed cell death. Mutations that cause a gain of ces-1 function or a reduction of ces-2 function prevent these cells, the sisters of the two pharyngeal NSM neurons, from dying. These mutations do not affect most other cell deaths. Genetic studies indicate that ces-1 and ces-2 affect the fates of the NSM sisters by regulating the genes required for all programmed cell deaths to occur.

1991 ◽  
Vol 331 (1261) ◽  
pp. 263-271 ◽  

During the course of normal embryonic and post-embryonic development, 131 cells in a Caenorhabditis elegans hermaphrodite undergo programmed cell death. Loss of function mutations in either of the genes ced-3 or ced-4 abolish cell deaths, enabling these ‘undead’ cells to survive and be incorporated into the adult with no obvious deleterious consequences. Ultrastructural reconstructions have shown that undead cells exhibit many differentiated characteristics. Most of the reconstructed cells appeared to be neurons with all the characteristic features associated with such cells, such as processes, synaptic vesicles and presynaptic specializations. However, clear morphological differences were seen among the undead neurons, suggesting a diversity of cell type. One of the reconstructed cells was a rectal epithelial cell, which had displaced its lineal sister that normally functions in this role. Removal of the ability to undergo programmed cell death by mutation therefore reveals a diversity of cryptic differentiated states that are acquired by cells that normally are destined to die.


Development ◽  
1982 ◽  
Vol 67 (1) ◽  
pp. 89-100
Author(s):  
Alison M. G. Robertson ◽  
J. N. Thomson

In the nematode C. elegans, cells undergoing programmed death in the developing ventral nerve cord were identified by Nomarski optics and prepared for ultrastructural study at various times after their birth in mitosis. The sequence of changes observed suggests that the hypodermis recognizes the dying cell before completion of telophase. The dying cell is engulfed and digestion then occurs until all that remains within the hypodermal cytoplasm is a collection of membranous whorls interspersed with condensed chromatin-like remnants. The process shares several features with apoptosis, the mode of programmed cell death observed in vertebrates and insects. The selection of cells for programmed death appears not to involve competition for peripheral targets.


1994 ◽  
Vol 345 (1313) ◽  
pp. 243-246 ◽  

During the development of the C. elegans hermaphrodite, 131 of the 1090 cells generated undergo programmed cell death. Genetic studies have identified mutations in 14 genes that specifically affect this process. These genes define a genetic pathway for programmed cell death in C. elegans . Two genes, ced-3 and ced-4 , are required for cells to undergo programmed cell death, while a third gene, ced-9 , protects cells that should live from undergoing programmed cell death. The proteins encoded by ced-3 and ced-9 show significant similarity to proteins that affect programmed cell death in vertebrates, suggesting that the molecular cell death pathway in which ced-3 , ced-4 , and ced-9 act has been conserved between nematodes and vertebrates.


Genetics ◽  
1991 ◽  
Vol 129 (1) ◽  
pp. 79-94 ◽  
Author(s):  
R E Ellis ◽  
D M Jacobson ◽  
H R Horvitz

Abstract After programmed cell death, a cell corpse is engulfed and quickly degraded by a neighboring cell. For degradation to occur, engulfing cells must recognize, phagocytose and digest the corpses of dying cells. Previously, three genes were known to be involved in eliminating cell corpses in the nematode Caenorhabditis elegans: ced-1, ced-2 and nuc-1. We have identified five new genes that play a role in this process: ced-5, ced-6, ced-7, ced-8 and ced-10. Electron microscopic studies reveal that mutations in each of these genes prevent engulfment, indicating that these genes are needed either for the recognition of corpses by other cells or for the initiation of phagocytosis. Based upon our study of double mutants, these genes can be divided into two sets. Animals with mutations in only one of these sets of genes have relatively few unengulfed cell corpses. By contrast, animals with mutations in both sets of genes have many unengulfed corpses. These observations suggest that these two sets of genes are involved in distinct and partially redundant processes that act in the engulfment of cell corpses.


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