Spaeny-Dekking L, Nilsson L, von Euler A, van de Putte P, Goosen N
Laboratory of Molecular Genetics, Leiden Institute of Chemistry, Gorlaeus Laboratories, Leiden University, The Netherlands.
Mol Gen Genet. 1995 Jan 20;246(2):259-65. doi: 10.1007/BF00294690.
The Escherichia coli Fis protein is known to be involved in a variety of processes, including the activation of stable RNA operons. In this paper we study the ability of a set of N-terminal Fis deletion mutants to stimulate transcription of the tRNA(2Ser) gene. The results indicate that the domain of the Fis protein containing residues 1-26 is not required for transcription activation. The Fis mutants that are still active in transcription stimulation can also complement the reduced growth rates of Fis- cells, suggesting that the same activating domain is involved in this phenomenon. In addition, we show that in fast growing cultures in the absence of an active Fis protein, minicells are formed. These minicells seem to arise from septum formation near the cell poles. Suppression of minicell formation by Fis also does not require the presence of the N-terminal domain of the protein.
已知大肠杆菌Fis蛋白参与多种过程，包括稳定RNA操纵子的激活。在本文中，我们研究了一组N端Fis缺失突变体刺激tRNA(2Ser)基因转录的能力。结果表明，Fis蛋白中包含第1至26位残基的结构域对于转录激活并非必需。在转录刺激中仍具有活性的Fis突变体也能够弥补Fis缺失细胞生长速率的降低，这表明相同的激活结构域参与了这一现象。此外，我们发现，在没有活性Fis蛋白的快速生长培养物中会形成微细胞。这些微细胞似乎源自细胞两极附近的隔膜形成。Fis对微细胞形成的抑制也不需要该蛋白N端结构域的存在。
