Disease relevance of tufA

• The nucleotide sequence of the cloned tufA gene of Escherichia coli [1].
• When the tufA gene of Escherichia coli was used as a probe in hybridization experiments, duplicate tuf genes were found in gram-negative bacteria from three major phyla: purple bacteria, bacteroides, and cyanobacteria [2].
• The sequence of the tufA gene from the extreme thermophilic eubacterium Thermus aquaticus EP 00276 was determined [3].
• We have cloned the tufA gene in a plasmid, containing the powerful major leftward promoter (PL) of phage lambda [4].
• Restriction endonuclease fragments of DNA from Neisseria gonorrhoeae and Chlamydia trachomatis (mouse pneumonitis biovar) were hybridized to probes from the N-terminal and C-terminal portions of the Escherichia coli tufA gene [5].

High impact information on tufA

• Together with targeted mutagenesis of the tufA gene, conditions were found to overcome membrane impermeability, thereby allowing the selection of three mutants harbouring elongation factor (EF)-Tu Arg230-->Cys, Arg333-->Cys or Thr334-->Ala which confer pulvomycin resistance [6].
• This gene maps in the same context as the tufA gene of Escherichia coli str operon [7].
• Eleven independently isolated insertions are described, six in tufA and five in tufB [8].
• Reverse transcription-PCR (RT-PCR) methods were developed for detecting mRNA from rpoH, groEL, and tufA genes. mRNA from all three genes was detected immediately after the cells had been killed by heat or ethanol but gradually disappeared with time when dead cells were held at room temperature [9].
• An M13-based genetic retrieval system reported by Zeef and Bosch [Mol. Gen. Genet. 238 (1993) 252-260] was used to segregate and identify an extremely growth-defective kirromycin-resistant (KrR) tufA mutation, encoding Gln124-->Lys (Q124K), from a KrR parent strain [10].

Biological context of tufA

• These plasmids continued to express tufA, as judged by the ability to complement mocimycin resistance and by electrophoretic analysis of synthesized proteins [11].
• Evidence for an internal promoter preceding tufA in the str operon of Escherichia coli [11].
• The mocimycin resistant phenotype is the result of mutations in each of two genes, tufA and tufB [12].
• The transcribed region of R03 showed extensive sequence homology with the Escherichia coli elongation factor gene, tufA [13].

Anatomical context of tufA

• Rates of growth, ribosome synthesis and elongation factor synthesis in a tufA defective strain of E. coli [14].

Other interactions of tufA

• Nucleotide differences between tufA and tufB were found at 13 positions [1].
• Measurements of transcription rates from various regions of the str operon in cells carrying the fus gene and the beginning of the tufA gene on a high copy number plasmid confirmed that transcription was initiated within a 600 bp EcoRI fragment in the distal portion of the fus gene [15].

Analytical, diagnostic and therapeutic context of tufA

• A deletion mutant of a plasmid born Escherichia coli tufA gene, which codes for a truncated elongation factor Tu comprising domains 2 and 3, has been constructed by genetic engineering [16].
• Both random and site-directed mutagenesis methods have yielded sets of purified mutant EF-Tu resistant to kirromycin (kirT) or pulvomycin (pulT) [17].

References