Casaregola S, D'Ari R, Huisman O
Mol Gen Genet. 1982;185(3):430-9. doi: 10.1007/BF00334135.
A recA::lac operon fusion was constructed using the phage Mu d(Ap, lac) in Escherichia coli to obtain precise measurements of the level of recA gene expression in various genetic backgrounds. The RecA protein normally represents 0.02% of total protein. This value is known to increase dramatically after treatments interrupting DNA synthesis; kinetic experiments showed that the rate of recA expression increases 17-fold within 10 min after UV irradiation or thymine starvation. In mutants affected in SOS regulation or repair the following observations were made: (i) the tif-1 mutation in the recA gene does not alter the basal level of recA expression, suggesting that it improves the protease activity of RecA; (ii) the lexA3 mutation does not create a "super-repressor" of recA; (iii) the tsl-1 mutation in the lexA gene makes the LexA protein a poor repressor of recA at 30 degrees C (2.5-fold derepression) and a poor substrate for RecA protease (3-fold stimulation of recA expression by UV); (iv) the spr-55 amber mutation in the lexA gene causes a 30-fold increase in recA expression, higher than all inducing treatments, and this level cannot be further increased by nalidixic acid; (v) the zab-53 mutation at the recA locus, known to abolish tsl-mediated induction of recA expression, is trans-recessive and thus probably affects a regulatory site on the DNA; (vi) uvrA, B and C, recB and recF mutations do not increase the basal level of recA expression, suggesting that there are not sufficient spontaneous lesions to cause induction even when any one of these three repair pathways is inoperative.
利用噬菌体Mu d(Ap, lac)在大肠杆菌中构建了recA::lac操纵子融合体,以精确测量recA基因在各种遗传背景下的表达水平。RecA蛋白通常占总蛋白的0.02%。已知在中断DNA合成的处理后,该值会急剧增加;动力学实验表明,紫外线照射或胸腺嘧啶饥饿后10分钟内,recA表达速率增加17倍。在SOS调控或修复受影响的突变体中,有以下观察结果:(i) recA基因中的tif-1突变不会改变recA表达的基础水平,这表明它提高了RecA的蛋白酶活性;(ii) lexA3突变不会产生recA的“超级阻遏物”;(iii) lexA基因中的tsl-1突变使LexA蛋白在30℃时成为recA的低效阻遏物(去阻遏2.5倍),并且是RecA蛋白酶的低效底物(紫外线照射后recA表达受刺激3倍);(iv) lexA基因中的spr-55琥珀突变导致recA表达增加30倍,高于所有诱导处理,并且这个水平不能被萘啶酸进一步提高;(v) recA位点的zab-53突变已知可消除tsl介导的recA表达诱导,它是反式隐性的,因此可能影响DNA上的一个调控位点;(vi) uvrA、B和C、recB和recF突变不会增加recA表达的基础水平,这表明即使这三种修复途径中的任何一种不起作用,也没有足够的自发损伤来引起诱导。