Homologous DNA interactions in the evolution of genes and species

1998年，小林在法国见到了拉德曼和科瓦尔奇科夫斯基。1998年，小林在美国见到了拉德曼。1999年，拉德曼访问日本，并在日本生物化学学会年会上发表演讲。1999年，Kowalczykowski访问日本并在3R研讨会上发表演讲。以下列出了主要来自小林实验室的成果，这些成果与此次合作关系最密切。(1)细菌中的同源重组与自私限制性修饰基因的相互作用。几个rec基因recA，recBC，ruvAB，ruvC，recG被发现通过修复切割的染色体来保护细菌免受RM基因复合物的侵害，如脉冲场凝胶电泳所检测到的。遗传分析表明，Chi序列与RecBCD酶的相互作用起着重要作用。在与Kowalczykowski实验室共同发表的一篇论文中，一种突变的RecBCD酶在体外序列识别中发生了改变。(2)通过B减轻和增强III型限制 ...更多信息 噬菌体和宿主同源重组功能。Rac原噬菌体的recET基因和λ噬菌体的red基因显示出减轻EcoP 1和EcoP 15的III型限制。相反，RecBCD途径刺激III型限制。(3)大肠杆菌重组缺陷突变体中巨大线性染色体的自发积累。通过脉冲场凝胶电泳在各种重组相关突变体中检测到大肠杆菌染色体的巨大线性形式，其由其环状形式的自发断裂产生。(4)为什么错配修复基因存在？一些细菌携带“孤儿”DNA甲基转移酶，不与限制酶配对。识别CC（A/T）GG的大肠杆菌K-12的一些菌株中的Dcm提供了一个实例。其作用尚不明确。我们证明，Dcm作为分子疫苗，保护基因组免受EcoRII（一种识别相同序列的RM系统）编程的分离后杀伤。(5)错配和同源重组。将“随机游走“模型推广到解释序列趋异和错配修复系统的影响。少

Kobayashi saw Radman and Kowalczykowski in France in 1998. Kobayashi saw Radman in USA in 1998. In 1999, Radman visited Japan and gave a lecture in the annual meeting of Biochemistry society of Japan. In 1999, Kowalczykowski visited Japan and gave a talk in 3R symposium. The following lists achievements, primarily from Kobayashi laboratory, which are most related to this collaboration.(1) Bacterial homologous recombination in fight and collaboration with selfish restriction modification genes. Several rec genes --- recA, recBC, ruvAB, ruvC, recG --- were found to defend bacteria against the RM gene complexes by repairing cleaved chromosomes, as detected by pulsed-field gel electrophoresis. Genetic analysis indicates that the interaction of Chi sequence with RecBCD enzyme, plays an important role. In a paper published together with Kowalczykowski lab, a mutant RecBCD enzyme was shown be altered in sequence recognition in vitro.(2) Alleviation and enhancement of type III restriction by b … More acteriophage and host homologous recombination functions. recET genes of Rac prophage and red genes of bacteriophage lambda were shown to alleviate type III restriction by EcoP1 and EcoP15. In contrast, RecBCD pathway stimulated type III restriction.(3) Spontaneous accumulation of huge linear chromosomes in recombination-defective mutants of Escherichia coli. Huge linear forms of E.coli chromosome that are produced by spontaneous breakage of its circular forms were detected by pulsed-field gel electrophoresis in various recombination-related mutants.(4) Why is a mismatch repair gene present? Some bacteria carry"orphan"DNA methyltransferase that is not paired with a restriction enzyme. Dcm in some strains of E.coli K-12 recognizing CC(A/T)GG provides one example. Its role has not been clear. We demonstrated that Dcm serves as molecular vaccine protecting the genome from post-segregational killing programmed by EcoRII, an RM system recognizing the same sequence.(5) Mismatch and homologous recombination. The"random walk"model was extended to explain the effects of sequence divergence and mismatch repair system. Less