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

Human immunodeficiency virus-1 (HIV-1) Vpr expression halts the proliferation of human cells at or near the G2cell-cycle checkpoint. The transition from G2to mitosis is normally controlled by changes in the state of phosphorylation and subcellular compartmentalization of key cell-cycle regulatory pr...

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Published inScience (American Association for the Advancement of Science) Vol. 294; no. 5544; pp. 1105 - 1108
Main Authors Carlos M. C. de Noronha, Sherman, Michael P., Lin, Harrison W., Cavrois, Marielle V., Moir, Robert D., Goldman, Robert D., Greene, Warner C.
Format Journal Article
LanguageEnglish
Published Washington, DC American Society for the Advancement of Science 02.11.2001
American Association for the Advancement of Science
The American Association for the Advancement of Science
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Summary:Human immunodeficiency virus-1 (HIV-1) Vpr expression halts the proliferation of human cells at or near the G2cell-cycle checkpoint. The transition from G2to 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 G2arrest, 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.
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ISSN:0036-8075
1095-9203
DOI:10.1126/science.1063957