Bruni R, Martin D, Jiricny J
Friedrich Miescher Institute, Basel, Switzerland.
Nucleic Acids Res. 1988 Jun 10;16(11):4875-90. doi: 10.1093/nar/16.11.4875.
The role of d(GATC) sites in determining the efficiency of methyl-directed mismatch repair in Escherichia coli was investigated. Transfection of host bacteria, both proficient and deficient in mismatch repair, with a series of artificially constructed M13 heteroduplexes showed that a decrease in the total number of d(GATC) sequences within these vectors lowered the efficiency of repair in vivo. Single hemimethylated d(GATC) sequences were still able to direct the correction event to the unmethylated strand, providing that the mismatch to d(GATC) site distance was shorter than approximately 1 kb. In excess of this distance, the effect of hemimethylated d(GATC) sites on mismatch correction was almost unnoticeable. The directionality of the repair event could be dictated by d(GATC) sequences situated both upstream and downstream of the mispair, suggesting that this important antimutagenic pathway can proceed bidirectionally.
研究了d(GATC)位点在确定大肠杆菌甲基定向错配修复效率中的作用。用一系列人工构建的M13异源双链体转染错配修复能力正常和缺陷的宿主细菌,结果表明这些载体中d(GATC)序列总数的减少会降低体内修复效率。只要错配与d(GATC)位点的距离短于约1 kb,单个半甲基化的d(GATC)序列仍能够将校正事件导向未甲基化链。超过此距离,半甲基化d(GATC)位点对错配校正的影响几乎不明显。修复事件的方向性可由错配上下游的d(GATC)序列决定,这表明这一重要的抗诱变途径可以双向进行。