Document Detail


Nuclear diacylglycerol kinase-zeta is a negative regulator of cell cycle progression in C2C12 mouse myoblasts.
MedLine Citation:
PMID:  17488950     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The nucleus contains diacylglycerol kinases (DGKs), i.e., the enzymes that, by converting diacylglycerol (DG) into phosphatidic acid, terminate DG-dependent events. It has been demonstrated that nuclear DGK-zeta interferes with cell cycle progression. We previously reported that nuclear DGK-zeta expression increased during myogenic differentiation, whereas its down-regulation impaired differentiation. Here, we evaluated the possible involvement of nuclear DGK-zeta in cell cycle progression of C2C12 myoblasts. Overexpression of a wild-type DGK-zeta, which mainly localized to the nucleus (but not of a kinase dead mutant or of a mutant that did not enter the nucleus), blocked the cells in the G1 phase of the cell cycle, as demonstrated by in situ analysis of biotinylated-16-dUTP incorporated into newly synthesized DNA and by flow cytometry. In contrast, down-regulation of endogenous DGK-zeta by short interfering RNA (siRNA) increased the number of cells in both the S and G2/M phases of the cell cycle. Cell cycle arrest of cells overexpressing wild-type DGK-zeta was accompanied by decreased levels of retinoblastoma protein phosphorylated on Ser-807/811. Down-regulation of endogenous DGK-zeta, using siRNA, prevented the cell cycle block characterizing C2C12 cell myogenic differentiation. Overall, our results identify nuclear DGK-zeta as a key determinant of cell cycle progression and differentiation of C2C12 cells.
Authors:
Camilla Evangelisti; Pier Luigi Tazzari; Massimo Riccio; Roberta Fiume; Yasukazu Hozumi; Federica Falà; Kaoru Goto; Lucia Manzoli; Lucio Cocco; Alberto M Martelli
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2007-05-08
Journal Detail:
Title:  FASEB journal : official publication of the Federation of American Societies for Experimental Biology     Volume:  21     ISSN:  1530-6860     ISO Abbreviation:  FASEB J.     Publication Date:  2007 Oct 
Date Detail:
Created Date:  2007-10-01     Completed Date:  2008-01-07     Revised Date:  2012-02-15    
Medline Journal Info:
Nlm Unique ID:  8804484     Medline TA:  FASEB J     Country:  United States    
Other Details:
Languages:  eng     Pagination:  3297-307     Citation Subset:  IM    
Affiliation:
Dipartimento di Scienze Anatomiche Umane e Fisiopatologia dell'Apparato Locomotore, Cell Signalling Laboratory, Università di Bologna, via Irnerio 48, 40126 Bologna, Italy.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Animals
Cell Cycle / physiology*
Cell Cycle Proteins / metabolism
Cell Differentiation*
Cell Line
Cell Nucleus / enzymology*
DNA Replication
Diacylglycerol Kinase / genetics,  metabolism*
Isoenzymes / genetics,  metabolism*
Mice
Myoblasts* / cytology,  enzymology,  physiology
RNA, Small Interfering / genetics,  metabolism
Recombinant Fusion Proteins / genetics,  metabolism
Retinoblastoma Protein / genetics,  metabolism
Chemical
Reg. No./Substance:
0/Cell Cycle Proteins; 0/Isoenzymes; 0/RNA, Small Interfering; 0/Recombinant Fusion Proteins; 0/Retinoblastoma Protein; EC 2.7.1.107/Diacylglycerol Kinase; EC 2.7.1.107/diacylglycerol kinase zeta, mouse

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


Previous Document:  Prevalence and risk factors of diabetic nephropathy in an urban South Indian population: the Chennai...
Next Document:  Inhibition of myoblast migration by prostacyclin is associated with enhanced cell fusion.