Dynamic disruptions in nuclear envelope architecture and integrity induced by HIV-1 Vpr

C. M C De Noronha, M. P. Sherman, H. W. Lin, M. V. Cavrois, R. D. Moir, R. D. Goldman, W. C. Greene*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

194 Scopus citations

Abstract

Human immunodeficiency virus-1 (HIV-1) Vpr expression halts the proliferation of human cells at or near the G2 cell-cycle checkpoint. The transition from G2 to mitosis is normally controlled by changes in the state of phosphorylation and subcellular compartmentalization of key cell-cycle regulatory proteins. In studies of the intracellular trafficking of these regulators, we unexpectedly found that wild-type Vpr, but not Vpr mutants impaired for G2 arrest, induced transient, localized herniations in the nuclear envelope (NE). These herniations were associated with defects in the nuclear lamina. Intermittently, these herniations ruptured, resulting in the mixing of nuclear and cytoplasmic components. These Vpr-induced NE changes probably contribute to the observed cell-cycle arrest.

Original languageEnglish (US)
Pages (from-to)1105-1108
Number of pages4
JournalScience
Volume294
Issue number5544
DOIs
StatePublished - Nov 2 2001

ASJC Scopus subject areas

  • General

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