Document Detail


Reversible shutdown of replicon initiation by transient hypoxia in Ehrlich ascites cells. Dependence of initiation on short-lived protein.
MedLine Citation:
PMID:  1360896     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The O2-dependent regulation of replication in Ehrlich ascites cells, characterized by a reversible shutdown of replicon initiation during hypoxia, was scrutinized with respect to the involvement of gene expression. Synchronous and asynchronous cells were subjected to transient hypoxia and examined for expression of selected 'late' growth-regulated mRNA and for the influence of inhibitors of transcription and translation on DNA replication. Irrespective of whether replicon initiation was suppressed by hypoxia or retriggered by reoxygenation, the levels of thymidine kinase mRNA and of proliferating cell-nuclear antigen/cyclin mRNA were as high as in untreated replicating cells. The level of histone H3.1 mRNA followed, with a distinct delay, the replicative activity of the cells governed by the imposed changes of pO2. The response of replication to inhibition of transcription and translation was virtually the same as to hypoxia, i.e. a selective suppression of replicon initiation. It was demonstrated that replicon initiation depends on one or several short-lived protein(s) (lifetime about 5 min) which is (are) formed under hypoxic conditions as well. The lifetime of the corresponding RNA message(s) is in the range of several hours. It is suggested that the expression of genes conditioning resting cells for DNA replication remains unaffected by hypoxia or by restoring the normal pO2. Hypoxic cell appear to rest in a state fully prepared for entering DNA replication, but a yet unknown event essential for replicon initiation is blocked. This event depends on a critical oxygen tension as well as on short-lived protein(s).
Authors:
H J Riedinger; V Gekeler; H Probst
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  European journal of biochemistry / FEBS     Volume:  210     ISSN:  0014-2956     ISO Abbreviation:  Eur. J. Biochem.     Publication Date:  1992 Dec 
Date Detail:
Created Date:  1993-01-11     Completed Date:  1993-01-11     Revised Date:  2007-07-23    
Medline Journal Info:
Nlm Unique ID:  0107600     Medline TA:  Eur J Biochem     Country:  GERMANY    
Other Details:
Languages:  eng     Pagination:  389-98     Citation Subset:  IM    
Affiliation:
Physiologisch-chemisches Institut, Universität Tübingen, Federal Republic of Germany.
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MeSH Terms
Descriptor/Qualifier:
Animals
Autoradiography
Carcinoma, Ehrlich Tumor / metabolism*
Cell Hypoxia
Cyclins / genetics
Cycloheximide / pharmacology
DNA Replication*
Dichlororibofuranosylbenzimidazole / pharmacology
Gene Expression
Nuclear Proteins / genetics
Oxygen / pharmacology*
Proliferating Cell Nuclear Antigen
Protein Biosynthesis / drug effects
RNA, Messenger / metabolism
Replicon / physiology*
Thymidine Kinase / genetics
Transcription, Genetic / drug effects
Chemical
Reg. No./Substance:
0/Cyclins; 0/Nuclear Proteins; 0/Proliferating Cell Nuclear Antigen; 0/RNA, Messenger; 53-85-0/Dichlororibofuranosylbenzimidazole; 66-81-9/Cycloheximide; 7782-44-7/Oxygen; EC 2.7.1.21/Thymidine Kinase

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


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