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首页> 外文期刊>Journal of Virology >Host-Mediated Repair of Discontinuities in DNA From T4 Bacteriophage
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Host-Mediated Repair of Discontinuities in DNA From T4 Bacteriophage

机译：来自T4噬菌体的DNA中不连续性的宿主介导的修复

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摘要

Discontinuities of T4 DNA which are caused by excision of UV-damaged areas, by decay of 32P atoms, or which are present in DNA from rII-ligam- phage produced in a host nonpermissive for amber mutants are all repaired by bacterial enzymes after infection in the presence of chloramphenicol. Escherichia coli DNA polymerase I participates in the host-mediated repair, but an approximately 20-fold variation in the levels of host polynucleotide ligase does not affect either the kinetics or the extent of repair observed. Upon removal of chloramphenicol, host-repaired DNA from UV-irradiated phage undergoes a secondary cycle of breakage, which ultimately results in solubilization of most of the phage DNA. If the cells are co-infected with nonirradiated helper phage, the secondary breaks are repaired and the continuity of the polynucleotide chain is restored. The close coincidence in the extent of primary and secondary breakage suggests that phage-coded enzymes recognize and excise areas improperly repaired by the host. In contrast to host-mediated repair, repair mediated by rescuing phage probably restored functionality to the damaged DNA.
机译：由紫外线损伤区域切除引起的T4 DNA的不连续，通过衰减 32-sup> p原子，或者从Rii - lig am中存在 - 在琥珀色突变体中宿主非疟疾中产生的噬菌体全部被氯霉素感染后的细菌酶修复。 大肠杆菌 DNA聚合酶I参与宿主介导的修复，但宿主多核苷酸连接酶水平的大约20倍的变化不会影响动力学或观察到的修复程度。除去氯霉素后，来自紫外线辐照噬菌体的宿主修复的DNA经历了次要的破损循环，最终导致大部分噬菌体DNA的溶解。如果细胞与非辐射辅助噬菌体共感染，则修复二次断裂，并且恢复多核苷酸链的连续性。初级和二次破裂程度密切巧合表明噬菌体编码的酶识别并由宿主修复不当的消费区。与宿主介导的修复相反，通过拯救噬菌体介导的修复可能恢复到受损的DNA的功能。

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