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Programmed cell death in the anuran tadpole tail requires expression of a cell surface glycoprotein
1Department of Biochemistry and Molecular Biology, Texas Tech University Health Sciences Center School of Medicine, Lubbock 79430, USA.
Abstract:
Programmed cell death is generally perceived as a suicide process involving activation of an internal death program thought to be common to all cells. We have previously presented evidence supporting the view that, at least in the tadpole tail, programmed cell death may involve assassination by cytotoxic cells such as resident macrophages. In this report, we show that regression of tadpole tail slices in culture is blocked by tunicamycin and brefeldin A, demonstrating that the intracellular protein trafficking machinery must be intact. Regression is also blocked by concanavalin A and fucose, suggesting a requirement for a cell surface glycoprotein. These observations are consistent with our hypothesis that programmed cell death requires expression of specific markers on the surfaces of cells destined to die, identifying the cells bearing those markers as targets for destruction.
Insights
Programmed cell death may not be suicide but assassination. Tadpole tail regression requires intact protein trafficking and cell surface glycoproteins, suggesting target cells are marked for destruction.
Area of Science:
- Developmental biology
- Cellular biology
- Immunology
Background:
- Programmed cell death (PCD) is traditionally viewed as a cellular suicide process.
- Previous research suggested PCD in tadpole tails might involve cytotoxic cells, like macrophages.
- This study investigates the cellular mechanisms underlying tadpole tail regression.
Purpose of the Study:
- To explore the mechanisms of programmed cell death in tadpole tail regression.
- To determine if intracellular protein trafficking is essential for PCD.
- To investigate the role of cell surface glycoproteins in identifying cells for destruction.
Main Methods:
- Organotypic culture of tadpole tail slices.
- Inhibition of intracellular protein trafficking using tunicamycin and brefeldin A.
- Inhibition of cell surface glycoprotein function using concanavalin A and fucose.
Main Results:
- Tadpole tail slice regression in culture was inhibited by tunicamycin and brefeldin A.
- Regression was also blocked by concanavalin A and fucose.
- These findings indicate the necessity of intact protein trafficking and cell surface glycoproteins.
Conclusions:
- Programmed cell death in tadpole tails appears to involve targeted destruction rather than simple suicide.
- Intact intracellular protein trafficking machinery is required for PCD.
- Specific cell surface glycoproteins may act as markers, identifying target cells for cytotoxic cells.