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[关于抑制基因stII突变体裂解缺陷的T4噬菌体突变的遗传与生理学研究]

[A genetic and physiologic study of mutations of T4 phage suppressing the lysis defect of gene stII mutants].

作者信息

Iankovskiĭ N K, Krylov V N

出版信息

Genetika. 1975;11(10):51-60.

PMID:773757
Abstract

A new gene rVI phage T4B is found. Mutations rVI belong to the class of r-mutations of T4B. Mutations rVI do not show the lysis inhibition after superinfection and determine the r-morphology of plaques on Escherichia coli CR63 lawn. Mutations rVI are gene-specific suppressors of stII lysis defect, but do not suppress the e lysis defect. Alleles rVI and rVI+ are co-dominated with regard to the ability to suppress the stII lysis defect. The suggest the stoichiometric character of rVI gene function. Mutations rVI increase the permeability of infected cells before the lysis. The gene rVI located between the genes 56 and 39 on the T4B genetic map, close to the gene 56. The still mutations described earlier (Krylov, Yankovsky, 1973) suppress the lysis defect of the am z25 mutant in the gene e. The suppression is manifested when infected bacteria develope only in the liquid media.

摘要

发现了一种新的基因rVI噬菌体T4B。rVI突变属于T4B的r突变类别。rVI突变在超感染后不表现出裂解抑制作用,并决定了在大肠杆菌CR63菌苔上噬菌斑的r形态。rVI突变是stII裂解缺陷的基因特异性抑制因子,但不抑制e裂解缺陷。就抑制stII裂解缺陷的能力而言,rVI和rVI +等位基因是共显性的。这表明rVI基因功能具有化学计量特征。rVI突变在裂解前增加了受感染细胞的通透性。rVI基因位于T4B遗传图谱上的基因56和39之间,靠近基因56。先前描述的静止突变(Krylov,Yankovsky,1973)抑制了基因e中am z25突变体的裂解缺陷。当受感染的细菌仅在液体培养基中生长时,这种抑制作用才会显现出来。

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