SPK-1, an SR protein kinase, inhibits programmed cell death in Caenorhabditis elegans
Name
Galvin-2011-Feb-SPK-1, an SR protein kinase, inhibits programmed cell death in Caenorhabditis elegans.pdf
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Author(s)
Galvin, Brendan D.
Denning, Daniel Prudden
Horvitz, Howard Robert
Date Issued
February 2011
Journal
Proceedings of the National Academy of Sciences of the United States of America
Publisher
National Academy of Sciences (U.S.)
Citation
Galvin, B. D., D. P. Denning, and H. R. Horvitz. “SPK-1, an SR Protein Kinase, Inhibits Programmed Cell Death in Caenorhabditis Elegans.” Proceedings of the National Academy of Sciences 108.5 (2011) : 1998-2003. ©2011 by the National Academy of Sciences.
Version
Final published version
Abstract
To identify genes involved in protecting cells from programmed cell death in Caenorhabditis elegans, we performed a genetic screen to isolate mutations that cause an increase in the number of programmed cell deaths. We screened for suppressors of the cell-death defect caused by a partial loss-of-function mutation in ced-4, which encodes an Apaf-1 homolog that promotes programmed cell death by activating the caspase CED-3. We identified one extragenic ced-4 suppressor, which has a mutation in the gene spk-1. The spk-1 gene encodes a protein homologous to serine-arginine-rich (SR) protein kinases, which are thought to regulate splicing. Previous work suggests that ced-4 can be alternatively spliced and that the splice variants function oppositely, with the longer transcript (ced-4L) inhibiting programmed cell death. spk-1 might promote cell survival by increasing the amount of the protective ced-4L splice variant. We conclude that programmed cell death in C. elegans is regulated by an alternative splicing event controlled by the SR protein kinase SPK-1.
MIT Department
Massachusetts Institute of Technology. Department of Biology
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DOI of Published Version
https://doi.org/10.1073/pnas.1018805108
