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

Janna M. Bigalke, Thomas Heuser, Daniela Nicastro, Ekaterina E. Heldwein

Research output: Contribution to journalArticlepeer-review

102 Scopus citations


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.

Original languageEnglish (US)
Article number4131
JournalNature communications
StatePublished - Jun 11 2014

ASJC Scopus subject areas

  • Chemistry(all)
  • Biochemistry, Genetics and Molecular Biology(all)
  • Physics and Astronomy(all)


Dive into the research topics of 'Membrane deformation and scission by the HSV-1 nuclear egress complex'. Together they form a unique fingerprint.

Cite this