Buoyant density studies of several mecillinam-resistant and division mutants of Escherichia coli.

Buoyant density studies of several mecillinam-resistant and division mutants of Escherichia coli.
复制标题

几种耐美西林和分裂大肠杆菌突变体的浮力密度研究。

DOI:
10.1128/jb.173.17.5396-5402.1991
复制
发表时间:
1991
影响因子:
3.2
通讯作者:
Higgins,ML
Higgins,ML
中科院分区:
生物学3区
文献类型:
--
作者:
Bylund,JE;Haines,MA;Walsh,K;Bouloc,P;D'Ari,R;Higgins,ML

文献摘要

相似文献

此前有报道称,野生型大肠杆菌细胞的浮力密度不会随生长速度、细胞大小或年龄而变化。在本报告中,我们使用Percoll梯度证实了这些发现,并分析了最近描述的LOV突变体,该突变体因对甲氧西林南的抗性而被选中,并被认为在质量增长和包膜合成之间的协调中受到影响。LOV突变细胞的平均浮力密度显著低于野生型细胞。同样,在美西林存在的情况下,野生型细胞的浮力密度降低。LOV突变体的密度和野生型一样,在2.8倍的生长速度范围内保持不变。然而,在这个范围内,平均细胞体积也是恒定的。对个体培养中浮力密度与细胞体积的函数关系的分析表明,较小的(新生)LOV突变细胞的密度高于较大的(老年)细胞;然而,小细胞的密度从未接近野生型细胞的密度,其密度与细胞大小(年龄)无关。在携带甲氧西林耐药突变pbpA(Ts)和RodA(Ts)和分裂突变FTSI(Ts)的细胞中,以及在用美西林处理的野生型细胞中,观察到了与LOV突变细胞相似的模式,但在对甲氧西林耐药的CRP或cyA突变体中没有观察到这种模式。
The buoyant density of wild-type Escherichia coli cells has previously been reported not to vary with growth rate and cell size or age. In the present report we confirm these findings, using Percoll gradients, and analyze the recently described lov mutant, which was selected for its resistance to mecillinam and has been suggested to be affected in the coordination between mass growth and envelope synthesis. The average buoyant density of lov mutant cells was significantly lower than that of wild-type cells. Similarly, the buoyant density of wild-type cells decreased in the presence of mecillinam. The density of the lov mutant, like that of the wild type, was invariant over a 2.8-fold range in growth rate. In this range, however, the average cell volume was also constant. Analysis of buoyant density as a function of cell volume in individual cultures revealed that smaller (newborn) lov mutant cells had higher density than larger (old) cells; however, the density of the small cells never approached that of the wild-type cells, whose density was independent of cell size (age). A pattern similar to that of lov mutant cells was observed in cells carrying the mecillinam-resistant mutations pbpA(Ts) and rodA(Ts) and the division mutation ftsI(Ts) at nonpermissive temperatures as well as in wild-type cells treated with mecillinam, but not in mecillinam-resistant crp or cya mutants.