Article abstract


Nature Neuroscience 12, 1534 - 1541 (2009)
Published online: 15 November 2009 | doi:10.1038/nn.2446

Glial precursors clear sensory neuron corpses during development via Jedi-1, an engulfment receptor

Hsiao-Huei Wu1,5, Elena Bellmunt2,6, Jami L Scheib1,6, Victor Venegas3,6, Cornelia Burkert1, Louis F Reichardt4, Zheng Zhou3, Isabel Fariñas2 & Bruce D Carter1


During the development of peripheral ganglia, 50% of the neurons that are generated undergo apoptosis. How the massive numbers of corpses are removed is unknown. We found that satellite glial cell precursors are the primary phagocytic cells for apoptotic corpse removal in developing mouse dorsal root ganglia (DRG). Confocal and electron microscopic analysis revealed that glial precursors, rather than macrophages, were responsible for clearing most of the dead DRG neurons. Moreover, we identified Jedi-1, an engulfment receptor, and MEGF10, a purported engulfment receptor, as homologs of the invertebrate engulfment receptors Draper and CED-1 expressed in the glial precursor cells. Expression of Jedi-1 or MEGF10 in fibroblasts facilitated binding to dead neurons, and knocking down either protein in glial cells or overexpressing truncated forms lacking the intracellular domain inhibited engulfment of apoptotic neurons. Together, these results suggest a cellular and molecular mechanism by which neuronal corpses are culled during DRG development.

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  1. The Center for Molecular Neuroscience, Kennedy Center For Human Development, and Department of Biochemistry, Vanderbilt University Medical School, Nashville, Tennessee, USA.
  2. Department de Biología Celular and CIBERNED, Universidad de Valencia, Burjassot, Spain.
  3. Verna and Marrs McLean Department of Biochemistry and Molecular Biology, Baylor College of Medicine, Houston, Texas, USA.
  4. Department of Physiology, University of California, San Francisco, California, USA.
  5. Present address: Department of Cell and Neurobiology, Keck School of Medicine of the University of Southern California, California, USA.
  6. These authors contributed equally to this work.

Correspondence to: Bruce D Carter1 e-mail: bruce.carter@vanderbilt.edu



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