Document Detail


The cyclin-dependent kinase inhibitors, cki-1 and cki-2, act in overlapping but distinct pathways to control cell cycle quiescence during C. elegans development.
MedLine Citation:
PMID:  19597327     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Cyclin-dependent kinase inhibitors (CKIs) are major contributors to the decision to enter or exit the cell cycle. The Caenorhabditis elegans genome encodes two CKIs belonging to the Cip/Kip family, cki-1 and cki-2. cki-1 has been shown to act as a canonical negative regulator of cell cycle entry, while the role of cki-2 remains unclear. We identified cki-2 in a genome-wide RNAi screen to reveal genes essential for developmental cell cycle quiescence. Examination of cki-2 knockout animals revealed extra rounds of cell divisions, verifying a role in establishing or maintaining the temporary cell cycle arrest. Despite the overlapping defects, the pathways mediated by cki-1 and cki-2 are discrete since the extra cell phenotype conferred by a putative cki-2(null) mutation is enhanced upon additional loss of cki-1 activity. Moreover, the extra cell division defect of cki-2 is not increased with the additional loss of lin-35 Rb, as is seen with cki-1. Thus, both cki-1 and cki-2 mediate cell cycle quiescence, but our genetic and phenotypic analyses demonstrate that they act within distinct pathways to exert control over the cell cycle machinery.
Authors:
Sarah H Buck; Daniel Chiu; R Mako Saito
Related Documents :
10545247 - Cell cycling and cell enlargement in developing leaves of arabidopsis.
19341427 - Distinct roles of the mtor components rictor and raptor in mo7e megakaryocytic cells.
14556967 - Induction of cell cycle regulatory proteins by murine b cell proliferating pectic polys...
20196847 - Sulforaphane induces cell cycle arrest by protecting rb-e2f-1 complex in epithelial ova...
21783997 - Disruption of gap junctional intercellular communication by antibiotic gentamicin is as...
11089927 - Postnatal differentiation of merkel cells in the rat palatine mucosa, with special refe...
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2009-08-25
Journal Detail:
Title:  Cell cycle (Georgetown, Tex.)     Volume:  8     ISSN:  1551-4005     ISO Abbreviation:  Cell Cycle     Publication Date:  2009 Aug 
Date Detail:
Created Date:  2009-08-17     Completed Date:  2009-10-27     Revised Date:  2011-09-26    
Medline Journal Info:
Nlm Unique ID:  101137841     Medline TA:  Cell Cycle     Country:  United States    
Other Details:
Languages:  eng     Pagination:  2613-20     Citation Subset:  IM    
Affiliation:
Department of Genetics, Dartmouth Medical School, Hanover, NH 03755, USA.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Animals
Animals, Genetically Modified
Caenorhabditis elegans / embryology*
Caenorhabditis elegans Proteins / genetics,  physiology*
Cell Cycle / genetics,  physiology*
Cyclin-Dependent Kinase Inhibitor Proteins / genetics,  physiology*
Gene Expression Regulation, Developmental / genetics,  physiology
Mutation
Phenotype
Polymerase Chain Reaction
RNA, Bacterial
Grant Support
ID/Acronym/Agency:
GM077031/GM/NIGMS NIH HHS; R01 GM077031-02/GM/NIGMS NIH HHS
Chemical
Reg. No./Substance:
0/Caenorhabditis elegans Proteins; 0/Cyclin-Dependent Kinase Inhibitor Proteins; 0/RNA I; 0/RNA, Bacterial; 0/cki-1 protein, C elegans; 0/cki-2 protein, C elegans
Comments/Corrections
Comment In:
Cell Cycle. 2009 Nov 1;8(21):3433-4   [PMID:  19823011 ]

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


Previous Document:  Suppression of metastasis of human breast cancer cells by chitosan oligosaccharides.
Next Document:  Role of the protein kinase Kin1 and nuclear centering in actomyosin ring formation in fission yeast.