首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >RESTRICTION-MODIFICATION SYSTEMS AS GENOMIC PARASITES IN COMPETITION FOR SPECIFIC SEQUENCES
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RESTRICTION-MODIFICATION SYSTEMS AS GENOMIC PARASITES IN COMPETITION FOR SPECIFIC SEQUENCES

机译:竞争修饰系统作为特定序列的基因型寄生虫

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Restriction-modification (RM) systems are believed to have evolved to protect cells from foreign DNA. However, this hypothesis may not be sufficient to explain the diversity and specificity in sequence recognition, as well as other properties, of these systems. We report that the EcoRI restriction endonuclease-modification methylase (rm) gene pair stabilizes plasmids that tarry it and that this stabilization is blocked by an RM of the same sequence specificity (EcoRI or its isoschizomer, Rsr I) but not by an RM of a different specificity (PaeR7I) on another plasmid. The PaeR7I rm likewise stabilizes plasmids, unless an rm gene pair with identical sequence specificity is present. Our analysis supports the following model for stabilization and incompatibility: the descendants of cells that have lost an rm gene pair expose the recognition sites in their chromosomes to lethal attack by any remaining restriction enzymes unless modification by another RM system of the same specificity protects these sites. Competition for specific sequences among these selfish genes may have generated the great diversity and specificity in sequence recognition among RM systems. Such altruistic suicide strategies, similar to those found in virus-infected cells, may have allowed selfish RM systems to spread by effectively competing with other selfish genes. [References: 46]
机译:据信限制性修饰(RM)系统已进化为保护细胞免受外源DNA侵害。但是,这种假设可能不足以解释这些系统在序列识别以及其他特性方面的多样性和特异性。我们报告说,EcoRI限制性核酸内切酶修饰甲基化酶(rm)基因对稳定了拖延它的质粒,并且该稳定作用被具有相同序列特异性的RM(EcoRI或其同分异构体,Rsr I)阻断,但未被a的RM阻断。在另一个质粒上具有不同的特异性(PaeR7I)。 PaeR7I rm同样可稳定质粒,除非存在具有相同序列特异性的rm基因对。我们的分析为稳定和不相容性提供了以下模型:丢失rm基因对的细胞后代会将其染色体上的识别位点暴露于任何剩余的限制性酶的致命攻击下,除非另一个具有相同特异性的RM系统对其进行修饰可以保护这些位点。这些自私的基因之间对特定序列的竞争可能在RM系统之间产生了巨大的多样性和特异性。这种无私的自杀策略,类似于在病毒感染的细胞中发现的策略,可能已通过与其他自私基因有效竞争而使自私RM系统得以传播。 [参考:46]

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