例如:"lncRNA", "apoptosis", "WRKY"

The Cell Death Pathway Regulates Synapse Elimination through Cleavage of Gelsolin in Caenorhabditis elegans Neurons.

Cell Rep. 2015 Jun 23;11(11):1737-48. Epub 2015 Jun 11
Lingfeng Meng 1 , Ben Mulcahy 2 , Steven J Cook 3 , Marianna Neubauer 4 , Airong Wan 1 , Yishi Jin 5 , Dong Yan 6
Lingfeng Meng 1 , Ben Mulcahy 2 , Steven J Cook 3 , Marianna Neubauer 4 , Airong Wan 1 , Yishi Jin 5 , Dong Yan 6
+ et al

[No authors listed]

Author information
  • 1 Department of Molecular Genetics and Microbiology, Duke University Medical Center, Research Drive, Durham, NC 27710, USA.
  • 2 Lunenfeld-Tanenbaum Research Institute, Toronto, ON M5G 1X5, Canada.
  • 3 Dominick P. Purpura Department of Neuroscience, Albert Einstein College of Medicine, Bronx, NY 10461, USA.
  • 4 Department of Physics and Center for Brain Science, Harvard University, Cambridge, MA 02138, USA.
  • 5 Neurobiology Section, Division of Biological Sciences, University of California, San Diego, La Jolla, CA 92093, USA; Department of Cellular and Molecular Medicine, School of Medicine, University of California, San Diego, La Jolla, CA 92093, USA; Howard Hughes Medical Institute, Chevy Chase, MD 20815, USA.
  • 6 Department of Molecular Genetics and Microbiology, Duke University Medical Center, Research Drive, Durham, NC 27710, USA; Department of Neurobiology and Duke Institute for Brain Sciences, Duke University Medical Center, Research Drive, Durham, NC 27710, USA. Electronic address: dong.yan@duke.edu.

摘要


Synapse elimination occurs in development, plasticity, and disease. Although the importance of synapse elimination has been documented in many studies, the molecular mechanisms underlying this process are unclear. Here, using the development of C. elegans RME neurons as a model, we have uncovered a function for the apoptosis pathway in synapse elimination. We find that the conserved apoptotic cell death (CED) pathway and axonal mitochondria are required for the elimination of transiently formed clusters of presynaptic components in RME neurons. This function of the CED pathway involves the activation of the actin-filament-severing protein, GSNL-1. Furthermore, we show that caspase CED-3 cleaves GSNL-1 at a conserved C-terminal region and that the cleaved active form of GSNL-1 promotes its actin-severing ability. Our data suggest that activation of the CED pathway contributes to selective elimination of synapses through disassembly of the actin filament network.