Document Detail


Mutations in String/CDC25 inhibit cell cycle re-entry and neurodegeneration in a Drosophila model of Ataxia telangiectasia.
MedLine Citation:
PMID:  18408079     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Mutations in ATM (Ataxia telangiectasia mutated) result in Ataxia telangiectasia (A-T), a disorder characterized by progressive neurodegeneration. Despite advances in understanding how ATM signals cell cycle arrest, DNA repair, and apoptosis in response to DNA damage, it remains unclear why loss of ATM causes degeneration of post-mitotic neurons and why the neurological phenotype of ATM-null individuals varies in severity. To address these issues, we generated a Drosophila model of A-T. RNAi knockdown of ATM in the eye caused progressive degeneration of adult neurons in the absence of exogenously induced DNA damage. Heterozygous mutations in select genes modified the neurodegeneration phenotype, suggesting that genetic background underlies variable neurodegeneration in A-T. The neuroprotective activity of ATM may be negatively regulated by deacetylation since mutations in a protein deacetylase gene, RPD3, suppressed neurodegeneration, and a human homolog of RPD3, histone deacetylase 2, bound ATM and abrogated ATM activation in cell culture. Moreover, knockdown of ATM in post-mitotic neurons caused cell cycle re-entry, and heterozygous mutations in the cell cycle activator gene String/CDC25 inhibited cell cycle re-entry and neurodegeneration. Thus, we hypothesize that ATM performs a cell cycle checkpoint function to protect post-mitotic neurons from degeneration and that cell cycle re-entry causes neurodegeneration in A-T.
Authors:
Stacey A Rimkus; Rebeccah J Katzenberger; Anthony T Trinh; Gerald E Dodson; Randal S Tibbetts; David A Wassarman
Related Documents :
19147009 - The primary cilium coordinates signaling pathways in cell cycle control and migration d...
19331659 - A signature-based method for indexing cell cycle phase distribution from microarray pro...
12552999 - Different mechanisms of soy isoflavones in cell cycle regulation and inhibition of inva...
15369799 - Rapamycin causes activation of protein phosphatase-2a1 and nuclear translocation of pcn...
1562509 - Regulation of breast cancer cell cycle progression by growth factors, steroids and ster...
8608009 - Starting the cell cycle: what's the point?
7768559 - Influence of intracellular renin on heart cell communication.
18423769 - Diesel exhaust particles are mutagenic in fe1-mutamouse lung epithelial cells.
20945139 - Novel combinational treatment of cisplatin with cyclophilin a inhibitors in human hepto...
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.     Date:  2008-04-11
Journal Detail:
Title:  Genes & development     Volume:  22     ISSN:  0890-9369     ISO Abbreviation:  Genes Dev.     Publication Date:  2008 May 
Date Detail:
Created Date:  2008-05-02     Completed Date:  2008-06-30     Revised Date:  2011-11-02    
Medline Journal Info:
Nlm Unique ID:  8711660     Medline TA:  Genes Dev     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1205-20     Citation Subset:  IM    
Affiliation:
Department of Biomolecular Chemistry, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin 53706, USA.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Animals
Animals, Genetically Modified
Apoptosis / genetics,  physiology
Ataxia Telangiectasia / genetics*,  physiopathology
Cell Cycle / genetics*,  physiology
Cell Cycle Proteins / genetics,  metabolism
Cell Line
DNA Replication
DNA-Binding Proteins / genetics,  metabolism
Disease Models, Animal
Drosophila / genetics,  physiology,  ultrastructure
Drosophila Proteins / genetics*,  metabolism
Eye / metabolism,  ultrastructure
Female
Flow Cytometry
Fluorescent Antibody Technique
Green Fluorescent Proteins / genetics,  metabolism
Hu Paraneoplastic Encephalomyelitis Antigens / genetics,  metabolism
Humans
Male
Microscopy, Electron, Scanning
Microscopy, Electron, Transmission
Mutation*
Nerve Degeneration / genetics*,  physiopathology
Neurons / cytology,  metabolism,  ultrastructure
Protein Tyrosine Phosphatases / genetics*,  metabolism
Protein-Serine-Threonine Kinases / genetics,  metabolism
RNA Interference
Tumor Suppressor Proteins / genetics,  metabolism
Grant Support
ID/Acronym/Agency:
R01 GM 067868/GM/NIGMS NIH HHS; R01 NS059001/NS/NINDS NIH HHS
Chemical
Reg. No./Substance:
0/Cell Cycle Proteins; 0/DNA-Binding Proteins; 0/Drosophila Proteins; 0/ELAV protein, Drosophila; 0/Hu Paraneoplastic Encephalomyelitis Antigens; 0/Tumor Suppressor Proteins; 147336-22-9/Green Fluorescent Proteins; EC 2.7.11.1/Protein-Serine-Threonine Kinases; EC 2.7.11.1/ataxia telangiectasia mutated protein; EC 3.1.3.48/Protein Tyrosine Phosphatases; EC 3.1.3.48/stg protein, Drosophila
Comments/Corrections

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


Previous Document:  Repression of gene expression by unphosphorylated NF-kappaB p65 through epigenetic mechanisms.
Next Document:  VEGF-A, VEGFR-1, VEGFR-2 and Tie2 levels in plasma of premature infants: relationship to retinopathy...