- THIS ARTICLE
- Full Text
- Full Text (PDF)
-
All Versions of this Article:
genetics.107.072090v1
176/1/73 most recent - 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
- Reprints & Permissions
- CITING ARTICLES
- Citing Articles via HighWire
- Citing Articles via Google Scholar
- GOOGLE SCHOLAR
- Articles by Tallada, V. A.
- Articles by Hagan, I. M.
- Search for Related Content
- PUBMED
- PubMed Citation
- Articles by Tallada, V. A.
- Articles by Hagan, I. M.
Originally published as Genetics Published Articles Ahead of Print on April 3, 2007.
Genetics, Vol. 176, 73-83, May 2007, Copyright © 2007
doi:10.1534/genetics.107.072090
Suppression of the Schizosaccharomyces pombe cut12.1 Cell-Cycle Defect by Mutations in cdc25 and Genes Involved in Transcriptional and Translational Control
Victor A. Tallada, Alan J. Bridge1, Patrick A. Emery2 and Iain M. Hagan3
CRUK Cell Division Group, Paterson Institute for Cancer Research, University of Manchester, Manchester M20 4BX, United Kingdom
3 Corresponding author: CRUK Cell Division Group, Paterson Institute for Cancer Research, Wilmslow Rd., Manchester M20 4BX, United Kingdom.
E-mail: ihagan{at}picr.man.ac.uk
Cdc25 phosphatase primes entry to mitosis by removing the inhibitory phosphate that is transferred to mitosis promoting factor (MPF) by Wee1 related kinases. A positive feedback loop then boosts Cdc25 and represses Wee1 activities to drive full-scale MPF activation and commitment to mitosis. Dominant mutations in the Schizosaccharomyces pombe spindle pole body (SPB) component Cut12 enable cdc25.22 mutants to overcome a G2 arrest at 36° and enter mitosis. The recessive temperature-sensitive cut12.1 mutation results in the formation of monopolar spindles in which the spindle pole marker Sad1 is enriched on the nonfunctional SPB at 36°. We identified mutations at five loci that suppressed the lethality of the recessive cut12.1 mutation at 36° and conferred lethality at 20°. Three of the five mutations led to the formation of monopolar spindles at restrictive temperatures, affected cell size at commitment to mitosis, and generated multiple Sad1 foci at nuclear periphery. The five loci, tfb2.rt1, tfb5.rt5, pla1.rt3, rpl4301.rt4, and rot2.1, and multicopy suppressors, including tfb1+ and dbp10+, are involved in transcription, translation, or RNA processing, prompting us to establish that elevating Cdc25 levels with the dominant cdc25.d1 allele, suppressed cut12.1. Thus, rot mutants provide a further link between protein production and cell-cycle progression.
This article has been cited by other articles:
 |
|
 |
|
  V. A. Tallada, K. Tanaka, M. Yanagida, and I. M. Hagan The S. pombe mitotic regulator Cut12 promotes spindle pole body activation and integration into the nuclear envelope J. Cell Biol., June 1, 2009; 185(5): 875 - 888. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L. Lo Presti, M. Cockell, L. Cerutti, V. Simanis, and P. M. Hauser Functional Characterization of Pneumocystis carinii brl1 by Transspecies Complementation Analysis Eukaryot. Cell, December 1, 2007; 6(12): 2448 - 2452. [Abstract] [Full Text] [PDF]
|
|