Skip Navigation

This Article
Right arrow Print PDF (4067K)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
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 Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (28)
Right arrow Commercial Re-use Guidelines
for Open Access NAR Content
Google Scholar
Right arrow Articles by Parkes, V.
Right arrow Articles by Johnston, L. H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Parkes, V.
Right arrow Articles by Johnston, L. H.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Nucleic Acids Research, 1992, Vol. 20, No. 21 5617-5623
© 1992


MOLECULAR BIOLOGY

SPO12 and SIT4 suppress mutations in DBF2, which encodes a cell cycle protein kinase that is periodically expressed

Vincent Parkes+ and Leland H. Johnston*

Laboratory of Yeast Genetics, National Institute for Medical Research Mill Hill, London NW7 1AA, UK

* To whom correspondence should be addressed

Received August 21, 1992. Revised October 1, 1992. Accepted October 1, 1992.

To help clarify the role of DBF2, a previously described cell cycle protein kinase, high copy number suppressors of the dbf2 mutation were isolated. Three open reading frames (ORF) have been identified. One ORF encodes a protein which has homology to a human small nuclear riboprotein, while the remaining two are genes which have been identified previously, SIT4 and SPO12. SIT4 is known to have a role in the cell cycle but the nature of the interaction between SIT4 and dbf2 is unclear. SPO12 has until now been implicated exclusively in meiosis. However, we show that SPO12 is expressed during vegetative growth, moreover it is expressed under cell cycle control coordinately with DBF2. SPO12 is a nonessential gene, but it becomes essential in a DBF2 delete genetic background. Furthermore, detailed analysis of the cell cycle of SPO12 delete cells revealed a small but significant delay in mitosis. Therefore, SPO12 does have a role during vegetative growth and it probably functions in mitosis in association with DBF2.


+ Present address: Molecular Cell Pathology, Royal Free Hospital School of Medicine, Rowland Hill Street, London NW3 2PF, UK


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
Mol. Biol. CellHome page
V. Reiser, K. E. D'Aquino, L.-S. Ee, and A. Amon
The Stress-activated Mitogen-activated Protein Kinase Signaling Cascade Promotes Exit from Mitosis
Mol. Biol. Cell, July 1, 2006; 17(7): 3136 - 3146.
[Abstract] [Full Text] [PDF]


Home page
Genes Dev.Home page
D. D'Amours and A. Amon
At the interface between signaling and executing anaphase--Cdc14 and the FEAR network
Genes & Dev., November 1, 2004; 18(21): 2581 - 2595.
[Abstract] [Full Text] [PDF]


Home page
Mol. Biol. CellHome page
R. Visintin, F. Stegmeier, and A. Amon
The Role of the Polo Kinase Cdc5 in Controlling Cdc14 Localization
Mol. Biol. Cell, November 1, 2003; 14(11): 4486 - 4498.
[Abstract] [Full Text] [PDF]


Home page
GeneticsHome page
R. Shah, S. Jensen, L. M. Frenz, A. L. Johnson, and L. H. Johnston
The Spo12 Protein of Saccharomyces cerevisiae: A Regulator of Mitotic Exit Whose Cell Cycle-Dependent Degradation Is Mediated by the Anaphase-Promoting Complex
Genetics, November 1, 2001; 159(3): 965 - 980.
[Abstract] [Full Text] [PDF]


Home page
GeneticsHome page
L. H. Rutkowski and R. E. Esposito
Recombination Can Partially Substitute for SPO13 in Regulating Meiosis I in Budding Yeast
Genetics, August 1, 2000; 155(4): 1607 - 1621.
[Abstract] [Full Text]


Home page
Mol. Biol. CellHome page
M. E. Grether and I. Herskowitz
Genetic and Biochemical Characterization of the Yeast Spo12 Protein
Mol. Biol. Cell, November 1, 1999; 10(11): 3689 - 3703.
[Abstract] [Full Text]


Home page
Microbiol. Mol. Biol. Rev.Home page
M. D. Mendenhall and A. E. Hodge
Regulation of Cdc28 Cyclin-Dependent Protein Kinase Activity during the Cell Cycle of the Yeast Saccharomyces cerevisiae
Microbiol. Mol. Biol. Rev., December 1, 1998; 62(4): 1191 - 1243.
[Abstract] [Full Text] [PDF]


Home page
Mol. Biol. CellHome page
S. L. Jaspersen, J. F. Charles, R. L. Tinker-Kulberg, and D. O. Morgan
A Late Mitotic Regulatory Network Controlling Cyclin Destruction in Saccharomyces cerevisiae
Mol. Biol. Cell, October 1, 1998; 9(10): 2803 - 2817.
[Abstract] [Full Text]


Home page
Mol. Cell. Biol.Home page
S. I. Komarnitsky, Y.-C. Chiang, F. C. Luca, J. Chen, J. H. Toyn, M. Winey, L. H. Johnston, and C. L. Denis
DBF2 Protein Kinase Binds to and Acts through the Cell Cycle-Regulated MOB1 Protein
Mol. Cell. Biol., April 1, 1998; 18(4): 2100 - 2107.
[Abstract] [Full Text]


Home page
Mol. Biol. CellHome page
B. L. Aerne, A. L. Johnson, J. H. Toyn, and L. H. Johnston
Swi5 Controls a Novel Wave of Cyclin Synthesis in Late Mitosis
Mol. Biol. Cell, April 1, 1998; 9(4): 945 - 956.
[Abstract] [Full Text]


Home page
Mol. Biol. CellHome page
F. C. Luca and M. Winey
MOB1, an Essential Yeast Gene Required for Completion of Mitosis and Maintenance of Ploidy
Mol. Biol. Cell, January 1, 1998; 9(1): 29 - 46.
[Abstract] [Full Text]


Home page
Genes Dev.Home page
J D Donovan, J H Toyn, A L Johnson, and L H Johnston
P40SDB25, a putative CDK inhibitor, has a role in the M/G1 transition in Saccharomyces cerevisiae.
Genes & Dev., July 15, 1994; 8(14): 1640 - 1653.
[Abstract] [PDF]


Home page
J. Biol. Chem.Home page
S. R. Chaves and G. Blobel
Nuclear Import of Spo12p, a Protein Essential for Meiosis
J. Biol. Chem., May 18, 2001; 276(21): 17712 - 17717.
[Abstract] [Full Text] [PDF]



Disclaimer:
Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.