QUICK SEARCH:   [advanced] Author: Keyword(s):
Home     Help     Feedback     Subscriptions     Archive     Search     Table of Contents

First published online November 17, 2003
doi: 10.1242/10.1242/dev.00855

This Article Figures Only Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Ohlmeyer, J. T. Articles by Schüpbach, T. Search for Related Content PubMed PubMed Citation Articles by Ohlmeyer, J. T. Articles by Schüpbach, T. Social Bookmarking                         What's this?

Encore facilitates SCF-Ubiquitin-proteasome-dependent proteolysis during Drosophila oogenesis

HHMI/Molecular Biology Department, Princeton University, Princeton, NJ 08544, USA

^* Author for correspondence (e-mail: gschupbach{at}molbio.princeton.edu)

Accepted 10 September 2003

Exit from the cell cycle requires the downregulation of Cyclin/Cdk activity. In the ovary of Drosophila, Encore activity is necessary in the germline to exit the division program after four mitotic divisions. We find that in encore mutant germaria, Cyclin A persists longer than in wild type. In addition, Cyclin E expression is not downregulated after the fourth mitosis and accumulates in a polyubiquitinated form. Mutations in genes coding for components of the SCF pathway such as cul1, UbcD2 and effete enhance the extra division phenotype of encore. We show that Encore physically interacts with the proteasome, Cul1 and Cyclin E. The association of Cul1, phosphorylated Cyclin E and the proteasome 19S-RP subunit S1 with the fusome is affected in encore mutant germaria. We propose that in encore mutant germaria the proteolysis machinery is less efficient and, in addition, reduced association of Cul1 and S1 with the fusome may compromise Cyclin E destruction and consequently promote an extra round of mitosis.

Key words: Mitosis, Encore, Oogenesis, Cyclin E, SCF, Proteolysis, Drosophila

CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter    What's this?

This article has been cited by other articles:

				S. Szuplewski, T. Sandmann, V. Hietakangas, and S. M. Cohen Drosophila Minus is required for cell proliferation and influences Cyclin E turnover Genes & Dev., September 1, 2009; 23(17): 1998 - 2003. [Abstract] [Full Text] [PDF]

				J. P. Blumenstiel, A. C. Noll, J. A. Griffiths, A. G. Perera, K. N. Walton, W. D. Gilliland, R. S. Hawley, and K. Staehling-Hampton Identification of EMS-Induced Mutations in Drosophila melanogaster by Whole-Genome Sequencing Genetics, May 1, 2009; 182(1): 25 - 32. [Abstract] [Full Text] [PDF]

				K. Narbonne-Reveau and M. Lilly The Cyclin-dependent Kinase Inhibitor Dacapo Promotes Genomic Stability during Premeiotic S Phase Mol. Biol. Cell, April 1, 2009; 20(7): 1960 - 1969. [Abstract] [Full Text] [PDF]

				A. Simonsen, R. C. Cumming, K. Lindmo, V. Galaviz, S. Cheng, T. E. Rusten, and K. D. Finley Genetic Modifiers of the Drosophila Blue Cheese Gene Link Defects in Lysosomal Transport With Decreased Life Span and Altered Ubiquitinated-Protein Profiles Genetics, June 1, 2007; 176(2): 1283 - 1297. [Abstract] [Full Text] [PDF]

				J. Z. Morris, A. Hong, M. A. Lilly, and R. Lehmann twin, a CCR4 homolog, regulates cyclin poly(A) tail length to permit Drosophila oogenesis Development, March 15, 2005; 132(6): 1165 - 1174. [Abstract] [Full Text] [PDF]

				E. L. Snapp, T. Iida, D. Frescas, J. Lippincott-Schwartz, and M. A. Lilly The Fusome Mediates Intercellular Endoplasmic Reticulum Connectivity in Drosophila Ovarian Cysts Mol. Biol. Cell, October 1, 2004; 15(10): 4512 - 4521. [Abstract] [Full Text] [PDF]