Presumptive TRP channel CED-11 promotes cell volume decrease and facilitates degradation of apoptotic cells in
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Author(s)
Driscoll, Kaitlin Bridget
Stanfield, Gillian M.
Droste, Rita
Horvitz, Howard Robert
Date Issued
July 2017
Journal
Proceedings of the National Academy of Sciences
Publisher
National Academy of Sciences (U.S.)
Citation
Driscoll, Kaitlin et al. “Presumptive TRP Channel CED-11 Promotes Cell Volume Decrease and Facilitates Degradation of Apoptotic Cells inCaenorhabditis Elegans.” Proceedings of the National Academy of Sciences 114, 33 (July 2017): 8806–8811 © 2017 National Academy of Sciences
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Final published version
Abstract
Apoptotic cells undergo a series of morphological changes. These changes are dependent on caspase cleavage of downstream targets, but which targets are signifi cant and how they facilitate the death process are not well understood. In Caenorhabditis elegans an increase in the refractility of the dying cell is a hallmark morphological change that is caspase dependent. We identify a presumptive transient receptor potential (TRP) cation channel, CED-11, that acts in the dying cell to promote the increase in apoptotic cell refractility. CED-11 is required for multiple other morphological changes during apoptosis, including an increase in electron density as visualized by electron microscopy and a decrease in cell volume. In ced-11 mutants, the degradation of apoptotic cells is delayed. Mutation of ced-11 does not cause an increase in cell survival but can enhance cell survival in other cell-death mutants, indicating that ced-11 facilitates the death process. In short, ced-11 acts downstream of caspase activation to promote the shrinkage, death, and degradation of apoptotic cells. Keywords: TRP channel; apoptosis; C. elegans; cell volume; apoptotic volume decrease
MIT Department
Massachusetts Institute of Technology. Department of Biology
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DOI of Published Version
https://doi.org/10.1073/PNAS.1705084114
