Yahara Koji, Horie Ryota, Kobayashi Ichizo, Sasaki Akira
Laboratory of Social Genome Sciences, Department of Medical Genome Sciences, Graduate School of Frontier Science and Institute of Medical Science, University of Tokyo, Tokyo, Japan.
Genetics. 2007 May;176(1):513-26. doi: 10.1534/genetics.106.056150. Epub 2007 Apr 3.
The necessity to repair genome damage has been considered to be an immediate factor responsible for the origin of sex. Indeed, attack by a cellular restriction enzyme of invading DNA from several bacteriophages initiates recombinational repair by gene conversion if there is homologous DNA. In this work, we modeled the interaction between a bacteriophage and a bacterium carrying a restriction enzyme as antagonistic coevolution. We assume a locus on the bacteriophage genome has either a restriction-sensitive or a restriction-resistant allele, and another locus determines whether it is recombination/repair proficient or defective. A restriction break can be repaired by a co-infecting phage genome if one of them is recombination/repair proficient. We define the fitness of phage (resistant/sensitive and repair-positive/-negative) genotypes and bacterial (restriction-positive/-negative) genotypes by assuming random encounter of the genotypes, with given probabilities of single and double infections, and the costs of resistance, repair, and restriction. Our results show the evolution of the repair allele depends on b(1)/b(0), the ratio of the burst size b(1) under damage to host cell physiology induced by an unrepaired double-strand break to the default burst size b(0). It was not until this effect was taken into account that the evolutionary advantage of DNA repair became apparent.
修复基因组损伤的必要性被认为是导致有性生殖起源的直接因素。事实上,如果存在同源DNA,来自几种噬菌体的入侵DNA受到细胞限制酶的攻击会通过基因转换启动重组修复。在这项工作中,我们将噬菌体与携带限制酶的细菌之间的相互作用建模为拮抗协同进化。我们假设噬菌体基因组上的一个位点有一个限制敏感或限制抗性等位基因,另一个位点决定它是重组/修复 proficient 还是有缺陷。如果其中一个噬菌体基因组是重组/修复 proficient,那么限制断裂可以由共同感染的噬菌体基因组修复。我们通过假设基因型的随机相遇、给定的单感染和双感染概率以及抗性、修复和限制的成本,来定义噬菌体(抗性/敏感和修复阳性/阴性)基因型和细菌(限制阳性/阴性)基因型的适应性。我们的结果表明,修复等位基因的进化取决于b(1)/b(0),即未修复的双链断裂对宿主细胞生理造成损伤时的爆发大小b(1)与默认爆发大小b(0)的比值。直到考虑到这种效应,DNA修复的进化优势才变得明显。