Why spherical Escherichia coli dies: the inside story.

Why spherical Escherichia coli dies: the inside story.
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为什么球形大肠杆菌会死亡:内幕。

DOI:
10.1128/jb.01975-07
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发表时间:
2008
影响因子:
3.2
通讯作者:
Young,KevinD
Young,KevinD
中科院分区:
生物学3区
文献类型:
--
作者:
Young,KevinD

文献摘要

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It is remarkable how often what we think must be true is not. In this issue, Bendezú and de Boer (1) tackle a phenomenon that seemed to have a perfectly good explanation, only to find that another, more satisfying and more interesting mechanism is at work. The short story is that several methods used to force Escherichia coli to grow as spheres share a common mode of bacterial killing in which cell division is impeded because FtsZ is mislocalized. The mechanism by which this occurs is surprisingly different. The inner membrane grows faster than is required by the reduced surface area, and the excess membrane folds inward and may pinch off to form intracytoplasmic vesicles. These extraneous membrane surfaces compete for FtsZ and hinder it from initiating normal division. This description is satisfying because it unites several disparate observations and replaces a previous, more simplistic explanation. It is interesting because it identifies an unusual capability of the bacterial membrane and because it implies that syntheses of membrane and cell wall are not coregulated as strictly as previously believed.At issue is a simple observation. E. coli normally grows as a uniform, straight rod. However, after deletion or inhibition of one of a few genes or proteins, E. coli loses its rod shape and takes on a spherical form that continues to enlarge until the cell eventually lyses (Fig. 1). The process can be triggered (i) by deleting one or more of the mreBCD genes or by inhibiting the MreB protein with compound A22;(ii) by deleting the mrdA gene that encodes PBP 2, inactivating a temperature-sensitive version of this protein, or inactivating PBP 2 with the β-lactam antibiotic amdinocillin; or (iii) by inactivating a temperaturesensitive version of the RodA protein, encoded by the mrdB gene (Fig. 1A)(see references in reference 1). In all these cases, E. coli becomes spherical and dies. Nonetheless, longlived cultures of coccoidal E. coli can be derived after each of these treatments by manipulating the growth conditions or genetic background (Fig. 1B). The older observation that elevated FtsZ levels suppress death in most of these cases led to the following commonly invoked and straightforward explanation. For a given volume, a rod shape will have a smaller circumference than will a sphere. Thus, a rod requires less FtsZ to form an unbroken septal ring and, by this reasoning, when E. coli loses the ability to grow as a rod there is too little FtsZ to create a functional