Quiñones A, Piechocki R, Messer W
Wissenschaftsbereich Genetik, Martin-Luther-Universität, Halle, Saale, German Democratic Republic.
Mol Gen Genet. 1988 Jan;211(1):106-12. doi: 10.1007/BF00338400.
By promoter fusion to the galK gene and comparative S1 analysis we investigated the in vivo regulation of transcription of the dnaQ gene which encodes the epsilon-subunit of the DNA polymerase III holoenzyme carrying the 3'----5' exonucleolytic proofreading function. Induction of a mutagenic stress situation by treatment with the base analogue 2-aminopurine (2-AP) leads to an increase in dnaQ transcription. S1 mapping analysis of the two dnaQ transcripts revealed a differential promoter activation for this 2-AP induced increase in dnaQ transcription. In addition, a similar galK promoter fusion with the dnaN gene coding for the beta-subunit of the DNA polymerase III holoenzyme revealed that dnaN transcription is also 2-AP inducible as judged by galactokinase activity. This is the first evidence for the inducibility of dnaQ gene expression (and possibly of other genes of the DNA polymerase II holoenzyme) and is discussed in relation to DNA repair mechanisms.
通过将启动子与galK基因融合并进行比较S1分析,我们研究了dnaQ基因转录的体内调控情况,该基因编码具有3'→5'核酸外切校正功能的DNA聚合酶III全酶的ε亚基。用碱基类似物2-氨基嘌呤(2-AP)处理诱导诱变应激情况会导致dnaQ转录增加。对两种dnaQ转录本的S1定位分析揭示了这种2-AP诱导的dnaQ转录增加存在差异启动子激活。此外,与编码DNA聚合酶III全酶β亚基的dnaN基因进行类似的galK启动子融合表明,根据半乳糖激酶活性判断,dnaN转录也可被2-AP诱导。这是dnaQ基因表达(以及可能的DNA聚合酶II全酶的其他基因)可诱导性的首个证据,并结合DNA修复机制进行了讨论。