Köppen A, Krobitsch S, Thoms B, Wackernagel W
Genetik, Fachbereich Biologie, Universität Oldenburg, Germany.
Proc Natl Acad Sci U S A. 1995 Jul 3;92(14):6249-53. doi: 10.1073/pnas.92.14.6249.
The RecBCD enzyme of Escherichia coli promotes recombination preferentially at chi nucleotide sequences and has in vivo helicase and strong duplex DNA exonuclease (exoV) activities. The enzyme without the RecD subunit, as in a recD null mutant, promotes recombination efficiently but independently of chi and has no nucleolytic activity. Employing phage lambda red gam crosses, phage T4 2- survival measurements, and exoV assays, it is shown that E. coli cells in which RecBCD has extensive opportunity to interact with linear chi-containing DNA (produced by rolling circle replication of a plasmid with chi or by bleomycin-induced fragmentation of the cellular chromosome) acquire the phenotype of a recD mutant and maintain this for approximately 2 h. It is concluded that RecBCD is converted into RecBC during interaction with chi by irreversible inactivation of RecD. After conversion, the enzyme is released and initiates recombination on other DNA molecules in a chi-independent fashion. Overexpression of recD+ (from a plasmid) prevented the phenotypic change and providing RecD after the change restored chi-stimulated recombination. The observed recA+ dependence of the downregulation of exoV could explain the previously noted "reckless" DNA degradation of recA mutants. It is proposed that chi sites are regulatory elements for the RecBCD to RecBC switch and thereby function as cis- and trans-acting stimulators of RecBC-dependent recombination.
大肠杆菌的RecBCD酶优先在chi核苷酸序列处促进重组,并且在体内具有解旋酶和强大的双链DNA核酸外切酶(exoV)活性。没有RecD亚基的该酶,如在recD缺失突变体中,能有效促进重组,但与chi无关,且没有核酸酶活性。利用噬菌体λ red gam杂交、噬菌体T4 2 - 存活测量和exoV测定,结果表明,RecBCD有大量机会与含线性chi的DNA相互作用的大肠杆菌细胞(由含chi的质粒滚环复制产生或由博来霉素诱导的细胞染色体片段化产生)获得recD突变体的表型,并维持约2小时。得出的结论是,RecBCD在与chi相互作用期间通过RecD的不可逆失活转化为RecBC。转化后,该酶被释放,并以不依赖chi的方式在其他DNA分子上启动重组。recD +(来自质粒)的过表达阻止了表型变化,并且在变化后提供RecD可恢复chi刺激的重组。观察到的exoV下调对recA +的依赖性可以解释先前注意到的recA突变体的“鲁莽”DNA降解。有人提出,chi位点是RecBCD向RecBC转换的调节元件,因此作为RecBC依赖性重组的顺式和反式作用刺激物发挥作用。