Document Detail


An intrinsic cell cycle checkpoint pathway mediated by MEK and ERK in Drosophila.
MedLine Citation:
PMID:  17011495     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Cell cycle checkpoints are surveillance mechanisms that safeguard genome integrity. While the extrinsic pathways that halt the cell cycle in response to DNA damages have been well documented, the intrinsic pathways that ensure orderly progression of cell cycle events are not well understood. We demonstrate that Drosophila MEK and ERK constitute an essential intrinsic checkpoint pathway that restrains cell cycle progression in the absence of DNA damage and also responds to ionizing radiation to arrest the cell cycle. Embryos lacking MEK exhibit faster and extra division cycles and fail to undergo timely midblastula transition (MBT) or arrest following ionizing radiation. Conversely, constitutively activated MEK causes cell cycle arrest. Further, MEK activation in the early embryo is cell cycle-dependent and Raf independent and increases in response to ionizing radiation or in the absence of Chk1. Thus, MEK/ERK activation is required for multiple checkpoints and is essential for orderly cell cycle progression.
Authors:
Vladic Mogila; Fan Xia; Willis X Li
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Developmental cell     Volume:  11     ISSN:  1534-5807     ISO Abbreviation:  Dev. Cell     Publication Date:  2006 Oct 
Date Detail:
Created Date:  2006-10-02     Completed Date:  2006-11-13     Revised Date:  2011-07-28    
Medline Journal Info:
Nlm Unique ID:  101120028     Medline TA:  Dev Cell     Country:  United States    
Other Details:
Languages:  eng     Pagination:  575-82     Citation Subset:  IM    
Affiliation:
Department of Biomedical Genetics, University of Rochester Medical Center, Rochester, New York 14642, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Cell Cycle / physiology*
Drosophila / embryology,  genetics,  metabolism*,  radiation effects
Embryo, Nonmammalian
Enzyme Activation
Gene Expression Regulation, Enzymologic
Immunohistochemistry
Kinetics
Mitogen-Activated Protein Kinase Kinases / genetics,  metabolism*
Mitogen-Activated Protein Kinases / genetics,  metabolism*
Models, Biological
RNA, Messenger / biosynthesis
Radiation, Ionizing
Grant Support
ID/Acronym/Agency:
R01 GM065774-05/GM/NIGMS NIH HHS; R01 GM077046-03/GM/NIGMS NIH HHS; R01GM077046/GM/NIGMS NIH HHS; R01GM65774/GM/NIGMS NIH HHS
Chemical
Reg. No./Substance:
0/RNA, Messenger; EC 2.7.11.24/Mitogen-Activated Protein Kinases; EC 2.7.12.2/Mitogen-Activated Protein Kinase Kinases
Comments/Corrections

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


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