Van Houten B, Snowden A
Department of Pathology, University of Vermont, Burlington 05405-0068.
Bioessays. 1993 Jan;15(1):51-9. doi: 10.1002/bies.950150108.
During the process of E. coli nucleotide excision repair, DNA damage recognition and processing are achieved by the action of the uvrA, uvrB, and uvrC gene products. The availability of highly purified proteins has lead to a detailed molecular description of E. coli nucleotide excision repair that serves as a model for similar processes in eukaryotes. An interesting aspect of this repair system is the protein complex's ability to work on a vast array of DNA lesions that differ widely in their chemical composition and molecular architecture. Here we propose a model for damage recognition in which the UvrB protein serves as the component that confers enhanced specificity to a preincision complex. We hypothesize that one major determinant for the formation of a stable preincision complex appears to be the disruption of base stacking interactions by DNA lesions.
在大肠杆菌核苷酸切除修复过程中，DNA损伤的识别和处理是通过uvrA、uvrB和uvrC基因产物的作用来实现的。高度纯化的蛋白质的可得性使得对大肠杆菌核苷酸切除修复有了详细的分子描述，这为真核生物中的类似过程提供了一个模型。这个修复系统的一个有趣方面是蛋白质复合物能够作用于大量化学组成和分子结构差异很大的DNA损伤。在这里，我们提出了一个损伤识别模型，其中UvrB蛋白作为赋予切割前复合物增强特异性的成分。我们假设，形成稳定切割前复合物的一个主要决定因素似乎是DNA损伤对碱基堆积相互作用的破坏。
