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紫外线照射的大肠杆菌中两种分裂抑制途径。

Two pathways of division inhibition in UV-irradiated E. coli.

作者信息

Burton P, Holland I B

出版信息

Mol Gen Genet. 1983;190(2):309-14. doi: 10.1007/BF00330656.

Abstract

We have investigated the mechanism of division inhibition in E. coli following UV-irradiation or nalidixic acid treatment. After UV, two separate mechanisms, both dependent upon recA+, appear to block division. One mechanism is dependent upon sfiA and sfiB, is inhibited by low levels (4 micrograms/ml) of rifamycin and is expressed in tif mutants at 42 degrees C. The second mechanism is independent of sfiA, and sfiB, is resistant to rifamycin and does not occur in cells lacking DNA replication forks. We suggest that this second mechanism is the result of the failure to terminate DNA replication in inhibited cells. Nalidixic acid inhibition of cell division also appears to involve both mechanisms but as found previously replication forks are also necessary to induce the sfi pathway.

摘要

我们研究了紫外线照射或萘啶酸处理后大肠杆菌中分裂抑制的机制。紫外线照射后,两种独立的机制似乎都能阻止分裂,且这两种机制都依赖于recA+。一种机制依赖于sfiA和sfiB,会被低水平(4微克/毫升)的利福平抑制,并在42摄氏度的tif突变体中表达。第二种机制独立于sfiA和sfiB,对利福平有抗性,且在缺乏DNA复制叉的细胞中不会发生。我们认为,第二种机制是受抑制细胞中DNA复制未能终止的结果。萘啶酸对细胞分裂的抑制似乎也涉及这两种机制,但如先前发现的那样,复制叉对于诱导sfi途径也是必需的。

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