Document Detail


HIV-1 Vpr induces G2 cell cycle arrest in fission yeast associated with Rad24/14-3-3-dependent, Chk1/Cds1-independent Wee1 upregulation.
MedLine Citation:
PMID:  16968670     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Viral protein R (Vpr), an accessory protein of human immunodeficiency virus type 1 (HIV-1), induces the G2 cell cycle arrest in fission yeast for which host factors, such as Wee1 and Rad24, are required. Catalyzing the inhibitory phosphorylation of Cdc2, Wee1 is known to serve as a major regulator of G2/M transition in the eukaryotic cell cycle. It has been reported that the G2 checkpoint induced by DNA damage or incomplete DNA replication is associated with phosphorylation and upregulation of Wee1 for which Chk1 and Cds1 kinase is required. In this study, we demonstrate that the G2 arrest induced by HIV-1 Vpr in fission yeast is also associated with increase in the phosphorylation and amount of Wee1, but in a Chk1/Cds1-independent manner. Rad24 and human 14-3-3 appear to contribute to Vpr-induced G2 arrest by elevating the level of Wee1 expression. It appears that Vpr could cause the G2 arrest through a mechanism similar to, but distinct from, the physiological G2 checkpoint controls. The results may provide useful insights into the mechanism by which HIV-1 Vpr causes the G2 arrest in eukaryotic cells. Vpr may also serve as a useful molecular tool for exploring novel cell cycle control mechanisms.
Authors:
Naoto Matsuda; Hiroko Tanaka; Sanae Yamazaki; Jun-Ichiro Suzuki; Koichi Tanaka; Takeshi Yamada; Michiaki Masuda
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2006-08-30
Journal Detail:
Title:  Microbes and infection / Institut Pasteur     Volume:  8     ISSN:  1286-4579     ISO Abbreviation:  Microbes Infect.     Publication Date:  2006 Oct 
Date Detail:
Created Date:  2006-11-10     Completed Date:  2007-02-15     Revised Date:  2011-11-02    
Medline Journal Info:
Nlm Unique ID:  100883508     Medline TA:  Microbes Infect     Country:  France    
Other Details:
Languages:  eng     Pagination:  2736-44     Citation Subset:  IM    
Affiliation:
Department of Microbiology, Dokkyo Medical University School of Medicine, Kita-kobayashi 880, Mibu, Tochigi 321-0293, Japan.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
14-3-3 Proteins / metabolism
Cell Cycle Proteins / metabolism*,  physiology*
G2 Phase*
Gene Expression Regulation
Gene Products, vpr / genetics,  physiology*
HIV-1
Intracellular Signaling Peptides and Proteins / physiology*
Nuclear Proteins / metabolism*
Phosphorylation
Protein Kinases / physiology*
Protein-Tyrosine Kinases / metabolism*
Schizosaccharomyces / cytology,  genetics,  physiology*
Schizosaccharomyces pombe Proteins / metabolism*,  physiology*
Up-Regulation
vpr Gene Products, Human Immunodeficiency Virus
Chemical
Reg. No./Substance:
0/14-3-3 Proteins; 0/Cell Cycle Proteins; 0/Gene Products, vpr; 0/Intracellular Signaling Peptides and Proteins; 0/Nuclear Proteins; 0/Schizosaccharomyces pombe Proteins; 0/rad24 protein, S pombe; 0/vpr Gene Products, Human Immunodeficiency Virus; EC 2.7.-/Protein Kinases; EC 2.7.1.-/wee1 protein, S pombe; EC 2.7.10.1/Protein-Tyrosine Kinases; EC 2.7.11.1/Checkpoint kinase 1

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Intranasal administration of adjuvant-combined recombinant influenza virus HA vaccine protects mice ...
Next Document:  Activation of mitochondrial-driven apoptosis in skeletal muscle cells is not mediated by reactive ox...