Dynamic Disruptions in Nuclear Envelope Architecture and Integrity Induced by HIV-1 Vpr
2001; American Association for the Advancement of Science; Volume: 294; Issue: 5544 Linguagem: Inglês
10.1126/science.1063957
ISSN1095-9203
AutoresCarlos M. C. de Noronha, Michael P. Sherman, Harrison W. Lin, Marielle Cavrois, Robert D. Moir, Robert D. Goldman, Warner C. Greene,
Tópico(s)Genomics and Chromatin Dynamics
ResumoHuman 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.
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