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Dynamic Disruptions in Nuclear Envelope Architecture and Integrity Induced by HIV-1 Vpr

Science  02 Nov 2001:
Vol. 294, Issue 5544, pp. 1105-1108
DOI: 10.1126/science.1063957

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Abstract

Human immunodeficiency virus–1 (HIV-1) Vpr expression halts the proliferation of human cells at or near the G2cell-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.

  • * To whom correspondence should be addressed. E-mail: wgreene{at}gladstone.ucsf.edu

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