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Nat Commun. 2014 Jun 11;5:4131. doi: 10.1038/ncomms5131.

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

Author information

1
Department of Molecular Biology and Microbiology, Tufts University School of Medicine, Boston, Massachusetts 02111, USA.
2
1] Biology Department and Rosenstiel Basic Medical Sciences Research Center, Brandeis University, Waltham, Massachusetts 02453, USA [2].
3
Biology Department and Rosenstiel Basic Medical Sciences Research Center, Brandeis University, Waltham, Massachusetts 02453, USA.

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.

PMID:
24916797
PMCID:
PMC4105210
DOI:
10.1038/ncomms5131
[Indexed for MEDLINE]
Free PMC Article

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