Disease relevance of atpA

• In addition, comparison of the sequence of the atpCAB genes of S. pneumoniae R6 (Opts) and M222 (an OptR strain produced by interspecies recombination between pneumococcus and S. oralis), and S. oralis (OptR) revealed that, in M222, an interchange of atpC and atpA had occurred [1].
• Genetic complementation between two mutant unc alleles (unc A401 and unc D409) affecting the Fl portion of the magnesium ion-stimulated adenosine triphosphatase of Escherichia coli K12 [2].
• Use of lambda unc transducing bacteriophages in genetic and biochemical characterization of H+-ATPase mutants of Escherichia coli [3].
• The lambda phage was induced, and asnA+ transducing phage that carried unc were selected [3].
• Six members of the Enterococcus faecium species group (E. faecium, E. hirae, E. durans, E. villorum, E. mundtii, and E. ratti) showed > 99% 16S rRNA gene sequence similarity, but the highest value of atpA gene sequence similarity was only 89.9% [4].

High impact information on atpA

• Analysis of the regulatory region upstream of papA in DNAs isolated from phase off and phase on cell populations showed that two deoxyadenosine methylase (Dam) sites, GATC1028 and GATC1130, were present [5].
• We conclude that the replication fork usually proceeds counter-clockwise toward the unc operon in the earliest period of replication [6].
• Studies with lacZ operon fusions showed that the papB gene encoded a trans-active effector required for papA transcription [7].
• A mutant with lesions both in the papA and the papE genes does not mediate digalactoside-specific agglutination [8].
• A non-polar mutation early in the papA pilin gene abolishes formation of Pap pili but does not affect the degree of digalactoside-specific hemagglutination [8].

Chemical compound and disease context of atpA

• Valinomycin plus potassium also caused a rapid decrease in the intracellular levels of ATP of normal E. coli cells, but had little if any effect on the ATP levels of two mutants of E. coli carrying lesions in the energy-transducing ATP complex (unc mutants) [9].
• The mutation in strain KW-1 leading to more rapid growth on lactose was cotransducible with the asn and unc loci, at 83 min on the E. coli genetic map [10].
• Carbonyl cyanide-m-chlorophenyl hydrazone-resistant Escherichia coli mutant that exhibits a temperature-sensitive unc phenotype [11].
• In Escherichia coli wild-type cells and in ATPase-deficient cells (unc mutants), glucose was found to be transported mainly by an ATP-driven system [12].
• Dicyclohexylcarbodiimide-resistant mutants of Escherichia coli were isolated and characterized In one mutant the unc genes and affects the membrane-integrated part of the ATP synthetase [13].

Biological context of atpA

• A method was developed to incorporate mutant unc alleles into plasmids [14].
• Partial diploid strains were prepared in which the uncB402 allele was incorporated into the plasmid and the new unc mutation into the chromosome, or vice versa [14].
• Complementation between the mutant unc alleles was indicated by growth on succinate, growth yields on glucose, ATP-dependent transhydrogenase activities, ATP-induced atebrin-fluorescence quenching and oxidative-phosphorylation measurements [14].
• A genetic-complementation analysis, using partial diploid strains, showed that the new mutant allele, uncD409, is in a gene distinct from the other previously identified genes uncA, uncB and uncC [2].
• Analyses of a lacZ- papA gene fusion located a promoter upstream from papA within the cloned DNA [15].

Anatomical context of atpA

• At least in the case of the pair atpHA, coupling seems to involve facilitated binding of fresh ribosomes to the atpA translational initiation regions [16].
• Removal of the Mg2+-adenosine triphosphatase from membranes derived from the parental or an uncA strain caused a loss of energy-linked functions and a concomitant increase in the permeability of the membrane for protons [17].
• Manipulations of the proton gradient at the cell membrane of ATP synthase-deficient E. coli (unc-) revealed that this part of the energy compartment is not responsible for the starvation-induced stimulation of cyclase [18].
• Mutant strains of Escherichia coli male cells defective in Ca2+,Mg2+-dependent ATPase (unc) were constructed and tested for their ability to form a complex between sex pili and the filamentous phage fd under conditions where either the membrane potential or the cellular concentration of ATP was lowered [19].

Associations of atpA with chemical compounds

• Re-sequencing of DNA in the region coding for the peptide has resulted in two corrections: insertion of a cytosine before position 715 and deletion of a thymine at position 731 of the uncA gene [20].
• Induction of expression of the four unc genes by the addition of isopropyl-beta-D-thiogalactoside resulted in inhibition of growth [21].
• If cells from the latter strain are treated with arsenate, transport rates increase to the same levels as found in uncA cells [22].
• The resulting mutation AS12 had a polar effect on the unc operon: membranes of the mutant AS12 contained the dicyclohexylcarbodiimide-binding protein c and the protein a as sole subunits of the ATP synthase [23].
• Freshly harvested uncA cells transport purine nucleosides at a higher rate than cells from the isogenic strain containing a functional ATPase [22].

Other interactions of atpA

• There is particularly tight coupling between atpH and atpA [24].
• The deleterious effect was eliminated by making a nonpolar deletion in the upstream F0 gene uncB, or by cloning each of the uncA-uncG fusion genes onto a separate plasmid, removed from the F0 genes, thus demonstrating that the fusion genes were not primarily responsible for the proton permeability [25].

Analytical, diagnostic and therapeutic context of atpA

• Phylogeny and identification of Enterococci by atpA gene sequence analysis [4].
• The uncA gene from this revertant was amplified by PCR, and cloned into an expression plasmid [26].
• When carried on a plasmid, the mutation is dominant in complementation tests with all mutant unc alleles tested and when transformed into wild-type strain AN346, the mutation results in an uncoupled phenotype [27].

References