This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Pile, L. A.
Right arrow Articles by Wassarman, D. A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Pile, L. A.
Right arrow Articles by Wassarman, D. A.

Next Article 

Molecular and Cellular Biology, July 2002, p. 4965-4976, Vol. 22, No. 14
0270-7306/02/$04.00+0     DOI: 10.1128/MCB.22.14.4965-4976.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

The SIN3/RPD3 Deacetylase Complex Is Essential for G2 Phase Cell Cycle Progression and Regulation of SMRTER Corepressor Levels

Lori A. Pile,1 Erin M. Schlag,1 and David A. Wassarman1,2*

Cell Biology and Metabolism Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892,1 Department of Pharmacology, University of Wisconsin Medical School, Madison, Wisconsin 537062

Received 4 January 2002/ Returned for modification 12 February 2002/ Accepted 1 April 2002

The SIN3 corepressor and RPD3 histone deacetylase are components of the evolutionarily conserved SIN3/RPD3 transcriptional repression complex. Here we show that the SIN3/RPD3 complex and the corepressor SMRTER are required for Drosophila G2 phase cell cycle progression. Loss of the SIN3, but not the p55, SAP18, or SAP30, component of the SIN3/RPD3 complex by RNA interference (RNAi) causes a cell cycle delay prior to initiation of mitosis. Loss of RPD3 reduces the growth rate of cells but does not cause a distinct cell cycle defect, suggesting that cells are delayed in multiple phases of the cell cycle, including G2. Thus, the role of the SIN3/RPD3 complex in G2 phase progression appears to be independent of p55, SAP18, and SAP30. SMRTER protein levels are reduced in SIN3 and RPD3 RNAi cells, and loss of SMRTER by RNAi is sufficient to cause a G2 phase delay, demonstrating that regulation of SMRTER protein levels by the SIN3/RPD3 complex is a vital component of the transcriptional repression mechanism. Loss of SIN3 does not affect global acetylation of histones H3 and H4, suggesting that the G2 phase delay is due not to global changes in genome integrity but rather to derepression of SIN3 target genes.

* Corresponding author. Mailing address: Department of Pharmacology, University of Wisconsin Medical School, 1300 University Ave., Madison, WI 53706. Phone: (608) 262-6648. Fax: (608) 262-1257. E-mail: dawassarman{at}facstaff.wisc.edu.

Molecular and Cellular Biology, July 2002, p. 4965-4976, Vol. 22, No. 14
0022-538X/02/$04.00+0     DOI: 10.1128/MCB.22.14.4965-4976.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Katzenberger, R. J., Marengo, M. S., Wassarman, D. A. (2009). Control of Alternative Splicing by Signal-dependent Degradation of Splicing-regulatory Proteins. J. Biol. Chem. 284: 10737-10746 [Abstract] [Full Text]  
  • Farhana, L., Dawson, M. I., Leid, M., Wang, L., Moore, D. D., Liu, G., Xia, Z., Fontana, J. A. (2007). Adamantyl-Substituted Retinoid-Related Molecules Bind Small Heterodimer Partner and Modulate the Sin3A Repressor. Cancer Res. 67: 318-325 [Abstract] [Full Text]  
  • Foglietti, C., Filocamo, G., Cundari, E., De Rinaldis, E., Lahm, A., Cortese, R., Steinkuhler, C. (2006). Dissecting the Biological Functions of Drosophila Histone Deacetylases by RNA Interference and Transcriptional Profiling. J. Biol. Chem. 281: 17968-17976 [Abstract] [Full Text]  
  • Furuyama, T., Dalal, Y., Henikoff, S. (2006). Chaperone-mediated assembly of centromeric chromatin in vitro. Proc. Natl. Acad. Sci. USA 103: 6172-6177 [Abstract] [Full Text]  
  • Struffi, P., Arnosti, D. N. (2005). Functional Interaction between the Drosophila Knirps Short Range Transcriptional Repressor and RPD3 Histone Deacetylase. J. Biol. Chem. 280: 40757-40765 [Abstract] [Full Text]  
  • Cowley, S. M., Iritani, B. M., Mendrysa, S. M., Xu, T., Cheng, P. F., Yada, J., Liggitt, H. D., Eisenman, R. N. (2005). The mSin3A Chromatin-Modifying Complex Is Essential for Embryogenesis and T-Cell Development. Mol. Cell. Biol. 25: 6990-7004 [Abstract] [Full Text]  
  • Moehren, U., Dressel, U., Reeb, C. A., Vaisanen, S., Dunlop, T. W., Carlberg, C., Baniahmad, A. (2004). The highly conserved region of the co-repressor Sin3A functionally interacts with the co-repressor Alien. Nucleic Acids Res 32: 2995-3004 [Abstract] [Full Text]  
  • Maile, T., Kwoczynski, S., Katzenberger, R. J., Wassarman, D. A., Sauer, F. (2004). TAF1 Activates Transcription by Phosphorylation of Serine 33 in Histone H2B. Science 304: 1010-1014 [Abstract] [Full Text]  
  • Pile, L. A., Spellman, P. T., Katzenberger, R. J., Wassarman, D. A. (2003). The SIN3 Deacetylase Complex Represses Genes Encoding Mitochondrial Proteins: IMPLICATIONS FOR THE REGULATION OF ENERGY METABOLISM. J. Biol. Chem. 278: 37840-37848 [Abstract] [Full Text]  


Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»