scholarly journals RecA can stimulate the relaxation activity of topoisomerase I: Molecular basis of topoisomerase-mediated genome-wide transcriptional responses in Escherichia coli

2006 ◽  
Vol 35 (1) ◽  
pp. 79-86 ◽  
Author(s):  
A. R. Reckinger ◽  
K. S. Jeong ◽  
A. B. Khodursky ◽  
H. Hiasa
Keyword(s):  
Escherichia Coli ◽  
Molecular Basis ◽  
Topoisomerase I ◽  
Transcriptional Responses ◽  
Relaxation Activity ◽  
Genome Wide

scholarly journals Metabolic Engineering for l-Glutamine Overproduction by Using DNA Gyrase Mutations in Escherichia coli

2013 ◽  
Vol 79 (9) ◽  
pp. 3033-3039 ◽  
Author(s):  
Mikiro Hayashi ◽  
Kazuhiko Tabata
Keyword(s):  
Escherichia Coli ◽  
Metabolic Engineering ◽  
Topoisomerase I ◽  
Dna Gyrase ◽  
Chromosomal Dna ◽  
Topoisomerase Iv ◽  
Α Subunit ◽  
Content Type ◽  
Genome Wide ◽  
K 12

ABSTRACTAnl-glutamine-overproducing mutant of anEscherichia coliK-12-derived strain was selected from randomly mutagenized cells in the course ofl-alanyl-l-glutamine strain development. Genome-wide mutation analysis unveiled a novel mechanism forl-glutamine overproduction in this mutant. Three mutations were identified that are related to thel-glutamine overproduction phenotype, namely, an intergenic mutation in the 5′-flanking region ofyeiGand two nonsynonymous mutations ingyrA(Gly821Ser and Asp830Asn). Expression ofyeiG, which encodes a putative esterase, was enhanced by the intergenic mutation. The nonsynonymous mutations ingyrA, a gene that encodes the DNA gyrase α subunit, affected the DNA topology of the cells. Gyrase is a type II topoisomerase that adds negative supercoils to double-stranded DNA. When the opposing DNA-relaxing activity was enhanced by overexpressing topoisomerase I (topA) and topoisomerase IV (parCandparE), an increase inl-glutamine production was observed. These results indicate that a reduction of chromosomal DNA supercoils in the mutant caused an increase inl-glutamine accumulation. The mechanism underlying this finding is discussed in this paper. We also constructed anl-glutamine-hyperproducing strain by attenuating cellularl-glutamine degradation activity. Although the reconstituted mutant (withyeiGtogether withgyrA) produced 200 mMl-glutamine, metabolic engineering finally enabled construction of a mutant that accumulated more than 500 mMl-glutamine.

Genome-wide transcriptional responses of Escherichia coli to recombinant protein overproduction

2007 ◽  
Vol 131 (2) ◽  
pp. S17
Author(s):  
Min Jee Kim ◽  
Soo Jung Park ◽  
Doo-Byoung Oh ◽  
Hyun Ah Kang ◽  
Ohsuk Kwon
Keyword(s):  
Escherichia Coli ◽  
Recombinant Protein ◽  
Transcriptional Responses ◽  
Genome Wide ◽  
Protein Overproduction

scholarly journals Genome-Wide Transcriptional Responses of Escherichia coli K-12 to Continuous Osmotic and Heat Stresses

2008 ◽  
Vol 190 (10) ◽  
pp. 3712-3720 ◽  
Author(s):  
Thusitha S. Gunasekera ◽  
Laszlo N. Csonka ◽  
Oleg Paliy
Keyword(s):  
Oxidative Stress ◽  
Escherichia Coli ◽  
High Temperature ◽  
Osmotic Stress ◽  
Stress Responses ◽  
Transcriptional Responses ◽  
High Osmolarity ◽  
Genome Wide ◽  
K 12 ◽  
And Oxidative Stress

ABSTRACT Osmotic stress is known to increase the thermotolerance and oxidative-stress resistance of bacteria by a mechanism that is not adequately understood. We probed the cross-regulation of continuous osmotic and heat stress responses by characterizing the effects of external osmolarity (0.3 M versus 0.0 M NaCl) and temperature (43°C versus 30°C) on the transcriptome of Escherichia coli K-12. Our most important discovery was that a number of genes in the SoxRS and OxyR oxidative-stress regulons were up-regulated by high osmolarity, high temperature, or a combination of both stresses. This result can explain the previously noted cross-protection of osmotic stress against oxidative and heat stresses. Most of the genes shown in previous studies to be induced during the early phase of adaptation to hyperosmotic shock were found to be also overexpressed under continuous osmotic stress. However, there was a poorer overlap between the heat shock genes that are induced transiently after high temperature shifts and the genes that we found to be chronically up-regulated at 43°C. Supplementation of the high-osmolarity medium with the osmoprotectant glycine betaine, which reduces the cytoplasmic K+ pool, did not lead to a universal reduction in the expression of osmotically induced genes. This finding does not support the hypothesis that K+ is the central osmoregulatory signal in Enterobacteriaceae.

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