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噬菌体P1在大肠杆菌K-12的lon突变体中溶原化缺陷的机制。

Mechanism of defective lysogenization by phage P1 in a lon-mutant of Escherichia coli K-12.

作者信息

Takano T

出版信息

Microbiol Immunol. 1977 Oct 20;21(10):573-81. doi: 10.1111/j.1348-0421.1977.tb00325.x.

Abstract

Phage P1 cannot lysogenize a lon- mutant of Escherichia coli K-12, which is defective in the regulation of cellular division cycle to result in snake formation (14). P1 mutants, called P1pla, can lysogenize the lon- host. These mutations have been classified into two complementation groups: one is cis-dominant; the other is trans-dominant. A temperature-sensitive lon- mutant was isolated, which exhibited the lon- phenotype at 42 C but not at 33 C. A temperature-shift experiment of the P1-lysogenic derivative of the lon- ts mutant showed lysis of the culture and induction of the phage production. It is proposed that P1 plasmid may be under a certain regulatory circuit of the division cycle of the host bacterium by indirectly regulating the production of P1 immune repressor, or alternatively by directly derepressing the functions of P1 prophage.

摘要

噬菌体P1不能使大肠杆菌K-12的lon-突变体溶源化,该突变体在细胞分裂周期调控方面存在缺陷,会导致形成蛇形(14)。称为P1pla的P1突变体能够使lon-宿主溶源化。这些突变已被分为两个互补组:一个是顺式显性;另一个是反式显性。分离出一个温度敏感型lon-突变体,它在42℃时表现出lon-表型,但在33℃时不表现。对lon- ts突变体的P1溶源衍生物进行温度转换实验,结果显示培养物裂解并诱导噬菌体产生。有人提出,P1质粒可能通过间接调节P1免疫阻遏物的产生,或者通过直接解除P1原噬菌体的功能抑制,处于宿主细菌分裂周期的某种调控回路之下。

相似文献

7
Maintenance of bacteriophage P1 plasmid.噬菌体P1质粒的维持
J Virol. 1977 Sep;23(3):476-82. doi: 10.1128/JVI.23.3.476-482.1977.

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