scholarly journals Genes required for the engulfment of cell corpses during programmed cell death in Caenorhabditis elegans.

Genetics ◽  
1991 ◽  
Vol 129 (1) ◽  
pp. 79-94 ◽  
Author(s):  
R E Ellis ◽  
D M Jacobson ◽  
H R Horvitz
Keyword(s):  
Cell Death ◽  
Caenorhabditis Elegans ◽  
Programmed Cell Death ◽  
Nematode Caenorhabditis Elegans ◽  
Electron Microscopic ◽  
New Genes ◽  
Microscopic Studies ◽  
A Cell ◽  
Cell Corpse ◽  
Dying Cells

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.

Post-embryonic development in the ventral cord of Caenorhabditis elegans

1976 ◽  
Vol 275 (938) ◽  
pp. 287-297 ◽  
Keyword(s):  
Cell Death ◽  
Caenorhabditis Elegans ◽  
Programmed Cell Death ◽  
Embryonic Development ◽  
Nerve Cells ◽  
Ventral Cord ◽  
Larval Moult ◽  
A Cell

56 nerve cells are added to the ventral cord and associated ganglia of Caenorhabditis elegans at about the time of the first larval moult. These cells are produced by the uniform division of 13 neuroblasts followed by a defined pattern of cell deaths. Comparison with the data in the previous paper suggests that there is a relationship between the ancestry of a cell and its function. The significance of programmed cell death is discussed.

On the nature of undead cells in the nematode Caenorhabditis elegans

1991 ◽  
Vol 331 (1261) ◽  
pp. 263-271 ◽  
Keyword(s):  
Cell Death ◽  
Caenorhabditis Elegans ◽  
Epithelial Cell ◽  
Programmed Cell Death ◽  
Synaptic Vesicles ◽  
Loss Of Function ◽  
Cell Type ◽  
Nematode Caenorhabditis Elegans ◽  
Characteristic Features ◽  
Morphological Differences

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.

Cell death in normal and rough eye mutants of Drosophila

Development ◽  
1991 ◽  
Vol 113 (3) ◽  
pp. 825-839 ◽  
Author(s):  
T. Wolff ◽  
D.F. Ready
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Compound Eye ◽  
Cell Lineage ◽  
Cell Fates ◽  
Cone Cells ◽  
A Cell ◽  
Retinal Epithelium ◽  
Fly Eye ◽  
Dying Cells

The regular, reiterated cellular pattern of the Drosophila compound eye makes it a sensitive amplifier of defects in cell death. Quantitative and histological methods reveal a phase of cell death between 35 and 50 h of development which removes between 2 and 3 surplus cells per ommatidium. The timing of this epoch is consistent with cell death as the last fate to be specified in the progressive sequence of cell fates that build the ommatidium. An ultrastructural survey of cell death suggests dying cells in the fly eye have similarities as well as differences with standard descriptions of programmed cell death. A failure of cell death to remove surplus cells disorganizes the retinal lattice. A screen of rough eye mutants identifies two genes, roughest and echinus, required for the normal elimination of cells from the retinal epithelium. The use of an enhancer trap as a cell lineage marker shows that the cone cells, like other retinal cells, are not clonally related to each other or to their neighbors.

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
Keyword(s):  
Cell Death ◽  
Caenorhabditis Elegans ◽  
Programmed Cell Death ◽  
Nematode Caenorhabditis Elegans ◽  
Genetic Studies ◽  
C Elegans

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.

scholarly journals The Natural History of Uterine Leiomyomas: Light and Electron Microscopic Studies of Fibroid Phases, Interstitial Ischemia, Inanosis, and Reclamation

2013 ◽  
Vol 2013 ◽  
pp. 1-20 ◽  
Author(s):  
Gordon P. Flake ◽  
Alicia B. Moore ◽  
Deloris Sutton ◽  
Grace E. Kissling ◽  
John Horton ◽  
...  
Keyword(s):  
Cell Death ◽  
Uterine Leiomyomas ◽  
Electron Microscopic ◽  
Nutritional Deprivation ◽  
Limited Life ◽  
Microscopic Studies ◽  
History Of ◽  
End Stage ◽  
Dying Cells ◽  
Phagocytic Reaction

We propose, and offer evidence to support, the concept that many uterine leiomyomas pursue a self-limited life cycle. This cycle can be arbitrarily divided on the basis of morphologic assessment of the collagen content into 4 phases: (1) proliferation, (2) proliferation and synthesis of collagen, (3) proliferation, synthesis of collagen, and early senescence, and (4) involution. Involution occurs as a result of both vascular and interstitial ischemia. Interstitial ischemia is the consequence of the excessive elaboration of collagen, resulting in reduced microvascular density, increased distance between myocytes and capillaries, nutritional deprivation, and myocyte atrophy. The end stage of this process is an involuted tumor with a predominance of collagen, little to no proliferative activity, myocyte atrophy, and myocyte cell death. Since many of the dying cells exhibit light microscopic and ultrastructural features that appear distinct from either necrosis or apoptosis, we refer to this process as inanosis, because it appears that nutritional deprivation, or inanition, is the underlying cause of cell death. The disposal of myocytes dying by inanosis also differs in that there is no phagocytic reaction, but rather an apparent dissolution of the cell, which might be viewed as a process of reclamation as the molecular contents are reclaimed and recycled.

scholarly journals Lysosome Biogenesis Mediated by vps-18 Affects Apoptotic Cell Degradation in Caenorhabditis elegans

2009 ◽  
Vol 20 (1) ◽  
pp. 21-32 ◽  
Author(s):  
Hui Xiao ◽  
Didi Chen ◽  
Zhou Fang ◽  
Jing Xu ◽  
Xiaojuan Sun ◽  
...  
Keyword(s):  
Cell Death ◽  
Caenorhabditis Elegans ◽  
Programmed Cell Death ◽  
Direct Evidence ◽  
Apoptotic Cell ◽  
Apoptotic Cells ◽  
Lysosome Biogenesis ◽  
Cell Corpse ◽  
Lysosomal Protein

Appropriate clearance of apoptotic cells (cell corpses) is an important step of programmed cell death. Although genetic and biochemical studies have identified several genes that regulate the engulfment of cell corpses, how these are degraded after being internalized in engulfing cell remains elusive. Here, we show that VPS-18, the Caenorhabditis elegans homologue of yeast Vps18p, is critical to cell corpse degradation. VPS-18 is expressed and functions in engulfing cells. Deletion of vps-18 leads to significant accumulation of cell corpses that are not degraded properly. Furthermore, vps-18 mutation causes strong defects in the biogenesis of endosomes and lysosomes, thus affecting endosomal/lysosomal protein degradation. Importantly, we demonstrate that phagosomes containing internalized cell corpses are unable to fuse with lysosomes in vps-18 mutants. Our findings thus provide direct evidence for the important role of endosomal/lysosomal degradation in proper clearance of apoptotic cells during programmed cell death.

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