The residual repair capacity of xeroderma pigmentosum complementation group C fibroblasts is highly specific for transcriptionally active DNA.
The residual repair capacity of xeroderma pigmentosum complementation group C fibroblasts is highly specific for transcriptionally active DNA.
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DOI：
10.1093/nar/18.3.443
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发表时间：
1990-02
影响因子：
14.9
通讯作者：
J. Venema;A. V. Hoffen;A. Natarajan;A. A. Zeeland-A.;L. Mullenders
中科院分区：
文献类型：
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作者：
J. Venema;A. V. Hoffen;A. Natarajan;A. A. Zeeland-A.;L. Mullenders
我们已经测量了去除嘧啶二聚体在定义的DNA序列融合和积极增长的正常人和着色性干皮病互补组C（XP-C）成纤维细胞暴露于10 J/m2的紫外线照射。在正常成纤维细胞中，分别在照射后4小时和24小时内从转录活性腺苷脱氨酶（ADA）基因中去除45%和90%的二聚体。在完全位于转录单位内或部分位于ADA基因的3'侧翼区的片段中发现相等的修复效率。从二氢叶酸还原酶（DHFR）基因中去除二聚体的速率和程度与ADA基因非常相似。转录失活的754位点的修复效率较低：18%和52%的二聚体分别在4小时和24小时内被去除。尽管总体修复能力有限，但融合的XP-C成纤维细胞有效地从ADA和DHFR基因中去除二聚体：在24小时内分别约90%和50%。ADA基因的3'端与正常人成纤维细胞中一样有效地修复，但在位于DHFR基因和ADA基因5'端的DNA片段中修复效率较低。失活的754位点的修复不超过二聚体从整个基因组中去除的非常慢的速率。融合和活跃生长的XP-C细胞显示出ADA、DHFR和754基因的相似修复效率。我们的研究结果表明，存在两个独立的运作途径，直接修复嘧啶二聚体在活跃或不活跃的染色质。XP-C细胞失去了修复失活染色质的能力，但仍然能够修复活性染色质。
We have measured removal of pyrimidine dimers in defined DNA sequences in confluent and actively growing normal human and xeroderma pigmentosum complementation group C (XP-C) fibroblasts exposed to 10 J/m2 UV-irradiation. In normal fibroblasts 45% and 90% of the dimers are removed from the transcriptionally active adenosine deaminase (ADA) gene within 4 and 24 hours after irradiation respectively. Equal repair efficiencies are found in fragments located entirely within the transcription unit or partly in the 3' flanking region of the ADA gene. The rate and extent of dimer removal from the dihydrofolate reductase (DHFR) gene is very similar to that of the ADA gene. Repair of the transcriptionally inactive 754 locus is less efficient: 18% and 52% of the dimers are removed within 4 and 24 hours respectively. In spite of the limited overall repair capacity, confluent XP-C fibroblasts efficiently remove dimers from the ADA and DHFR genes: about 90% and 50% within 24 hours respectively. The 3' end of the ADA gene is repaired as efficiently as in normal human fibroblasts, but less efficient repair occurs in DNA fragments located in the DHFR gene and at the 5' end of the ADA gene. Repair of the inactive 754 locus does not exceed the very slow rate of dimer removal from the genome overall. Confluent and actively growing XP-C cells show similar efficiencies of repair of the ADA, DHFR and 754 genes. Our findings suggest the existence of two independently operating pathways directed towards repair of pyrimidine dimers in either active or inactive chromatin. XP-C cells have lost the capacity to repair inactive chromatin, but are still able to repair active chromatin.