Ceglowski P, Lüder G, Alonso J C
Max-Planck-Institut für Molekulare Genetik, Berlin.
Mol Gen Genet. 1990 Jul;222(2-3):441-5. doi: 10.1007/BF00633853.
A recE mutant (recE6) of Bacillus subtilis was constructed by insertion of a selectable marker into the recE coding region. The insertional inactivation of the recE gene renders cells very sensitive to DNA damaging agents and severely impairs intermolecular recombination, but does not markedly affect plasmid interstrand annealing and intramolecular recombination. The recE6 allele was then introduced into a set of DNA repair-deficient strains of B. subtilis. The removal of DNA damage by the recF, addA addB, recH, recL and recP gene products is strictly dependent on an active recE gene product (recE-dependent pathway). On the other hand, the increased sensitization to purine adducts in the uvrA42 recE6 and polA5 recE6 strains suggests that such lethal lesions may be removed either by the recE-dependent or by the recE-independent pathway.
通过将一个选择标记插入枯草芽孢杆菌的recE编码区构建了一个recE突变体(recE6)。recE基因的插入失活使细胞对DNA损伤剂非常敏感,并严重损害分子间重组,但对质粒链间退火和分子内重组没有明显影响。然后将recE6等位基因导入一组枯草芽孢杆菌的DNA修复缺陷菌株中。recF、addA addB、recH、recL和recP基因产物对DNA损伤的去除严格依赖于活性recE基因产物(recE依赖性途径)。另一方面,uvrA42 recE6和polA5 recE6菌株对嘌呤加合物的敏感性增加表明,此类致死性损伤可能通过recE依赖性途径或recE非依赖性途径去除。