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体内限制。五、通过受限的T4噬菌体DNA在大肠杆菌中引入SOS功能,以及SOS功能对限制的缓解作用。

Restriction in vivo. V. Introduction of SOS functions in Escherichia coli by restricted T4 phage DNA, and alleviation of restriction by SOS functions.

作者信息

Dharmalingam K, Goldberg E B

出版信息

Mol Gen Genet. 1980 Apr;178(1):51-8. doi: 10.1007/BF00267212.

Abstract

Degradation products of restricted T4 DNA induced filamentation, mutagenesis, and to a lesser extent, synthesis of recA protein in wild type cells but not in recA, lexA or recBC mutants of Escherichia coli. We conclude that the structural damage to the DNA caused by restriction cleavage and exonuclease V degradation can induce SOS functions. Degradation of restricted nonglycosylated T4 DNA by exonuclease V delayed cell division and induced filament formation and mutagenesis in lexA+ but not in lexA- cells. Delay of cell division was also dependent upon recA and recBC functions. Such degradation of DNA also dramatically increased mutagenesis in tif- Sfi- cells at 42 degrees. The synthesis of recA protein continued in the restricting host after infection by the monglucosylated T4 phage, but enhanced synthesis is not induced to the extent seen in SOS induced tif- cells grown at 42 degrees. We also found that restriction of nonglycosylated T4 was alleviated in UV irradiated cells. The UV induced alleviation of rgl and rK restriction depended upon post irradiation protein synthesis and was not observed in recA, lexA or recBC mutants.

摘要

限制性T4 DNA的降解产物在野生型细胞中诱导了丝状化、诱变,并且在较小程度上诱导了recA蛋白的合成,但在大肠杆菌的recA、lexA或recBC突变体中则没有。我们得出结论,由限制性切割和外切核酸酶V降解对DNA造成的结构损伤可诱导SOS功能。外切核酸酶V对限制性非糖基化T4 DNA的降解延迟了细胞分裂,并在lexA+细胞中诱导了丝状形成和诱变,但在lexA-细胞中则没有。细胞分裂的延迟也依赖于recA和recBC功能。这种DNA降解在42℃时也显著增加了tif-Sfi-细胞中的诱变。在被单糖基化T4噬菌体感染后,recA蛋白的合成在限制性宿主中持续进行,但增强合成的程度不如在42℃生长的SOS诱导的tif-细胞中所见。我们还发现,在紫外线照射的细胞中,非糖基化T4的限制作用得到缓解。紫外线诱导的rgl和rK限制的缓解依赖于照射后蛋白质的合成,并且在recA、lexA或recBC突变体中未观察到。

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