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ssnA基因的特性,该基因与大肠杆菌稳定期开始时细胞活力的下降有关。

Characterization of the ssnA gene, which is involved in the decline of cell viability at the beginning of stationary phase in Escherichia coli.

作者信息

Yamada M, Talukder A A, Nitta T

机构信息

Department of Biological Chemistry, Faculty of Agriculture, Yamaguchi University, Yamaguchi 753-8515, Japan.

出版信息

J Bacteriol. 1999 Mar;181(6):1838-46. doi: 10.1128/JB.181.6.1838-1846.1999.

Abstract

When grown in rich medium, Escherichia coli exhibits a drastic reduction of the number of viable cells at the beginning of stationary phase. The decline of cell viability was retarded by disruption of the ssnA gene, which was identified as a gene subject to RpoS-dependent negative regulation. Moreover, ssnA expression was induced at the time of decline of cell viability at early stationary phase. The viability decline was augmented in the rpoS background, and this augmentation was suppressed by ssnA mutation. Cloning of the ssnA gene in a multicopy plasmid, pBR322, caused small colony formation and slow growth in liquid medium. Cells harboring the ssnA clone showed aberrant morphology that included enlarged and filamentous shapes. The gene product was identified as a 44-kDa soluble protein, but its function could not be deduced by homology searching. From these results, we conclude that ssnA is expressed in response to a phase-specific signal(s) and that its expression level is controlled by RpoS, by a mechanism which may contribute to determination of cell number in the stationary phase.

摘要

在丰富培养基中生长时,大肠杆菌在稳定期开始时活细胞数量会急剧减少。ssnA基因的破坏会延缓细胞活力的下降,该基因被鉴定为受RpoS依赖性负调控的基因。此外,在稳定期早期细胞活力下降时会诱导ssnA表达。在rpoS背景下,活力下降加剧,而这种加剧被ssnA突变所抑制。将ssnA基因克隆到多拷贝质粒pBR322中会导致小菌落形成以及在液体培养基中生长缓慢。携带ssnA克隆的细胞表现出异常形态,包括细胞增大和呈丝状。该基因产物被鉴定为一种44 kDa的可溶性蛋白,但其功能无法通过同源性搜索推导得出。从这些结果我们得出结论,ssnA是响应阶段特异性信号而表达的,其表达水平受RpoS控制,其机制可能有助于确定稳定期的细胞数量。

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Adaptation of gene expression in stationary phase bacteria.静止期细菌中基因表达的适应性
Curr Opin Genet Dev. 1997 Oct;7(5):582-8. doi: 10.1016/s0959-437x(97)80003-2.
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GASPing for life in stationary phase.在稳定期挣扎求生。
Cell. 1996 Jul 26;86(2):181-4. doi: 10.1016/s0092-8674(00)80089-6.

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