Abstract：
:It is vital that embryonic stem (ES) cells, which give rise to the diverse tissues of the mature organism, maintain genetic stability. To understand mechanisms for the prevention and causation of chromosomal instability, we have used spectral karyotyping (SKY) to analyse ES cells from wild-type and repair-gene knockout mice. We chose cells deficient in Ku70 (DNA end joining), Xrcc2 (gene conversion), Ercc1 (single-strand annealing) and Csb (transcription-coupled repair) to represent potentially-important DNA repair pathways, plus an Xpc-deficient line to examine loss of global nucleotide excision repair (NER). Spontaneous and radiation (X-ray or alpha-particle)-induced chromosome changes were assessed to measure the influence of different levels of damage severity on response. We show that most repair pathways (except for global NER) protect against chromosome changes induced by ionizing radiations, while only homology-dependent pathways protect against spontaneous chromosomal change in ES cells. However, for a given level of damage, the prevalence of different types of changes alters in the different repair-deficient lines. Thus, loss of Ercc1, Csb or Ku70 leads to increased fragment formation, but loss of Xrcc2 promotes exchanges between chromosomes. Strikingly, we found that loss of the Csb gene function specifically protects ES cells from complex exchanges, suggesting a role for transcription-associated events in complex exchange formation.
journal_name
DNA Repair (Amst)journal_title
DNA repairauthors
Griffin C,Waard Hd,Deans B,Thacker Jdoi
10.1016/j.dnarep.2005.05.005keywords:
subject
Has Abstractpub_date
2005-08-15 00:00:00pages
1019-27issue
9eissn
1568-7864issn
1568-7856pii
S1568-7864(05)00117-5journal_volume
4pub_type
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