Wood S G, Ubasawa A, Martin D, Jiricny J
Nucleic Acids Res. 1986 Aug 26;14(16):6591-602. doi: 10.1093/nar/14.16.6591.
The efficiency of in vivo correction of five "mismatch analogues", incorporated into M13mp9 DNA, was studied in an attempt to elucidate the structural determinants required for mismatch recognition by the repair machinery of E. coli. Inosine was efficiently removed from an I/T mismatch, presumably by the action of hypoxanthine glycosylase. The mismatch analogues DI/T (DI = 7-deazainosine), Tu/C (Tu = tubercidin), N/C (N = nebularine) and DN/C (DN = 7-deazanebularine) were left largely unrepaired, giving rise to high yields of mutant phenotype. The efficiency of correction of these mismatch analogues could be correlated with their structure within the base-pair.
研究了掺入M13mp9 DNA中的五种“错配类似物”在体内的校正效率,以试图阐明大肠杆菌修复机制识别错配所需的结构决定因素。肌苷可能通过次黄嘌呤糖基化酶的作用从I/T错配中有效去除。错配类似物DI/T(DI = 7-脱氮肌苷)、Tu/C(Tu = 杀结核菌素)、N/C(N = 喷司他丁)和DN/C(DN = 7-脱氮喷司他丁)大部分未被修复,产生了高比例的突变表型。这些错配类似物的校正效率与其在碱基对中的结构相关。