Fijalkowska I, Jonczyk P, Ciesla Z
Institute of Biochemistry and Biophysics, Polish Academy of Sciences, Warsaw.
Mutat Res. 1989 Mar;217(2):117-22. doi: 10.1016/0921-8777(89)90063-3.
E. coli strains bearing the recA441 mutation and various mutations in the polA gene resulting in enzymatically well-defined deficiencies of DNA polymerase I have been constructed. It was found that the recA441 strains bearing either the polA1 or polA12 mutation causing deficiency of the polymerase activity of pol I are unable to grow at 42 degrees C on minimal medium supplemented with adenine, i.e., when the SOS response is continuously induced in strains bearing the recA441 mutation. Under these conditions the inhibition of DNA synthesis is followed in recA441 polA12 by DNA degradation and loss of cell viability. A similar lethal effect is observed with the recA730 polA12 mutant. The recA441 strain bearing the polA107 mutation resulting in the deficiency of the 5'-3' exonuclease activity of pol I shows normal growth under conditions of continuous SOS response. We postulate that constitutive expression of the SOS response leads to an altered requirement for the polymerase activity of pol I.
已经构建出携带recA441突变以及polA基因中各种突变的大肠杆菌菌株,这些突变导致DNA聚合酶I在酶活性方面有明确的缺陷。结果发现,携带导致pol I聚合酶活性缺陷的polA1或polA12突变的recA441菌株,在补充了腺嘌呤的基本培养基上于42℃无法生长,也就是说,当携带recA441突变的菌株中SOS反应持续被诱导时。在这些条件下,recA441 polA12中DNA合成的抑制之后会出现DNA降解和细胞活力丧失。recA730 polA12突变体也观察到类似的致死效应。携带导致pol I 5'-3'核酸外切酶活性缺陷的polA107突变的recA441菌株,在持续SOS反应的条件下显示正常生长。我们推测,SOS反应的组成型表达导致对pol I聚合酶活性的需求发生改变。