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Association between DNA cleavage during apoptosis and regions of chromatin replication
Author(s) -
Khodarev Nikolai N.,
Sokolova Irina A.,
Vaughan Andrew T.M.
Publication year - 1998
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/(sici)1097-4644(19980915)70:4<604::aid-jcb16>3.0.co;2-g
Subject(s) - chromatin , dna replication , replication protein a , dna , eukaryotic dna replication , cleavage (geology) , microbiology and biotechnology , replicon , dna polymerase ii , origin recognition complex , control of chromosome duplication , biology , dna clamp , chemistry , genetics , gene , dna binding protein , transcription factor , paleontology , reverse transcriptase , rna , plasmid , fracture (geology)
We have addressed the association between the site of DNA cleavage during apoptosis and DNA replication. DNA double strand breaks were introduced into chromatin containing pulse labeled nascent DNA by the induction of apoptosis or autocleavage of isolated nuclei. The location of these breaks in relation to nascent DNA were revealed by Bal 31 exonuclease digestion at the cut sites. Our data show that Bal31 accessible cut sites are directly linked to regions enriched in nascent DNA. We suggest that these regions coincide with the termini of replication domains, possibly linked by strong DNA‐matrix interactions with biophysically defined topological structures of 0.5 ‐ 1.3 Mbp in size. The 50 kbp fragments that are commonly observed as products of apoptosis are also enriched in nascent DNA within internal regions but not at their termini. It is proposed that these fragments contain a subset of replicon DNA that is excised during apoptosis through recognition of their weak attachment to the nuclear matrix within the replication domain.J. Cell. Biochem. 70:604‐615, 1998. © 1998 Wiley‐Liss, Inc. © 1998 Wiley‐Liss, Inc.