Clustered sites of DNA repair synthesis during early nucleotide excision repair in ultraviolet light-irradiated quiescent human fibroblasts.
Clustered sites of DNA repair synthesis during early nucleotide excision repair in ultraviolet light-irradiated quiescent human fibroblasts.
复制标题
紫外光照射的静止人类成纤维细胞中早期核苷酸切除修复过程中 DNA 修复合成的聚集位点。
DOI：
10.1006/excr.2002.5519
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发表时间：
2002
期刊：
影响因子：
--
通讯作者：
Hanawalt,Philip
中科院分区：
文献类型：
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作者：
Svetlova,Maria;Solovjeva,Lioudmila;Pleskach,Nadezhda;Yartseva,Natalia;Yakovleva,Tatyana;Tomilin,Nikolai;Hanawalt,Philip
The ubiquitous process of nucleotide excision repair includes an obligatory step of DNA repair synthesis (DRS) to fill the gapped heteroduplex following excision of a short (∼30-nucleotide) damaged single-strand fragment. Using 5-iododeoxyuridine to label repair patches during the first 10–60 min after UV irradiation of quiescent normal human fibroblasts we have visualized a limited number of discrete foci of DRS. These must reflect clusters of elementary DRS patches, since single patches would not be detected. The DRS foci are attenuated in normal cells treated with α-amanitin or in Cockayne syndrome (CS) cells, which are specifically deficient in the pathway of transcription-coupled repair (TCR). It is therefore likely that the clusters of DRS arise in chromatin domains within which RNA polymerase II transcription is compartmentalized. However, we also found significant suppression of DRS foci in xeroderma pigmentosum, complementation group C cells in which global genome repair (GGR) is defective, but TCR is normal. This suggests that the TCR is responsible for the DRS cluster formation in the absence of GGR. The residual foci detected in CS cells indicate that, even at early times following UV irradiation, GGR may open some chromatin domains for processive scanning and consequent DRS independent of transcription.
