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Membrane deformation and scission by the HSV-1 nuclear egress complex

Author

Listed:
  • Janna M. Bigalke

    (Tufts University School of Medicine)

  • Thomas Heuser

    (Brandeis University
    Present address: Electron Microscopy Facility, Campus Science Support Facilities, Campus Vienna Biocenter, Dr. Bohr-Gasse 3, 1030 Vienna, Austria)

  • Daniela Nicastro

    (Brandeis University)

  • Ekaterina E. Heldwein

    (Tufts University School of Medicine)

Abstract

The nuclear egress complex (NEC) of herpesviruses such as HSV-1 is essential for the exit of nascent capsids from the cell nucleus. The NEC drives nuclear envelope vesiculation in cells, but the precise budding mechanism and the potential involvement of cellular proteins are unclear. Here we report that HSV-1 NEC alone is sufficient for membrane budding in vitro and thus represents a complete membrane deformation and scission machinery. It forms ordered coats on the inner surface of the budded vesicles, suggesting that it mediates scission by scaffolding the membrane bud and constricting the neck to the point of scission. The inward topology of NEC-mediated budding in vitro resembles capsid budding into the inner nuclear membrane during HSV-1 infection and nuclear envelope vesiculation in NEC-transfected cells. We propose that the NEC functions as minimal virus-encoded membrane-budding machinery during nuclear egress and does not require additional cellular factors.

Suggested Citation

  • Janna M. Bigalke & Thomas Heuser & Daniela Nicastro & Ekaterina E. Heldwein, 2014. "Membrane deformation and scission by the HSV-1 nuclear egress complex," Nature Communications, Nature, vol. 5(1), pages 1-12, September.
  • Handle: RePEc:nat:natcom:v:5:y:2014:i:1:d:10.1038_ncomms5131
    DOI: 10.1038/ncomms5131
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