DNA fragmentation during apoptosis is caused by frequent single-strand cuts

Détails

ID Serval
serval:BIB_1CD97BFE1033
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
DNA fragmentation during apoptosis is caused by frequent single-strand cuts
Périodique
Nucleic Acids Research
Auteur(s)
Peitsch  M. C., Muller  C., Tschopp  J.
ISSN
0305-1048 (Print)
Statut éditorial
Publié
Date de publication
09/1993
Volume
21
Numéro
18
Pages
4206-9
Notes
Journal Article
Research Support, Non-U.S. Gov't --- Old month value: Sep 11
Résumé
One of the hallmarks of apoptosis is the digestion of genomic DNA by an endonuclease, generating a ladder of small fragments of double-stranded DNA. We have examined the nature of the DNA breaks produced in mouse thymocytes triggered to undergo apoptosis by steroids or by stimulation of the T cell receptor. Whereas the typical ladder pattern of oligonucleosomal fragments was observed after agarose gel electrophoresis, numerous single-strand cuts were detected after electrophoresis under denaturing conditions. Single-strand nicks were found to be very frequent in the internucleosomal regions, but also to occur in the core particle-associated DNA. An identical pattern of single-strand nicks was obtained when chromatin DNA was exposed to the single-strand cleaving deoxyribonuclease I. The nicked DNA fragments, extracted from apoptotic thymocytes, were sensitive to the action of S1-nuclease. We propose that DNA fragmentation induced during apoptosis is not due to a double-strand cutting enzyme as previously postulated, but rather is the result of single-strand breaks. This ensures the dissociation of the DNA molecule at sites where cuts are found within close proximity.
Mots-clé
Animals Antigens, CD3/physiology Apoptosis/drug effects/*genetics Cells, Cultured Computer Simulation *DNA Damage Dexamethasone/pharmacology Electrophoresis, Agar Gel Mice Signal Transduction
Pubmed
Web of science
Création de la notice
24/01/2008 16:18
Dernière modification de la notice
03/03/2018 14:33
Données d'usage