Disease relevance of fliM

• Sequence of the flaA (cheC) locus of Escherichia coli and discovery of a new gene [1].
• The nucleotide sequence of the Bacillus subtilis fliM gene has been determined [2].
• The flaA locus of Vibrio parahaemolyticus encodes one of the four polar flagellin genes, the flagellum-capping protein HAP2, and three additional flagellar genes [3].
• Two tandemly located flagellin genes, flaA and flaB, with 79% nucleotide sequence identity were identified in Aeromonas salmonicida A449 [4].
• The location of the T. denticola fliQ-flhA' genes differs from that of the corresponding T. pallidum and Borrelia burgdorferi genes which are present in the large fla or flgB flagellar operons, respectively [5].

High impact information on fliM

• To facilitate kinetic and genetic studies, a phenotypic reporter of virulence was engineered by fusing flaA promoter sequences to a gene encoding green fluorescent protein [6].
• The V. parahaemolyticus polar flaC flagellin gene was poorly expressed in Escherichia coli Production of FlaC was stimulated by provision of the flaA locus in trans [3].
• Expression in a non-motile S. typhimurium fliN mutant restores motility but not chemotaxis, although expression in a non-motile E. coli fliM mutant does not restore motility [7].
• We cloned 17 fliM mutants, each defective in switching and having a point mutation at a different location, and then overexpressed and purified their products [8].
• However, we were unable to determine the nucleotide sequence of flaA upstream of amino acid 10 [9].

Chemical compound and disease context of fliM

• Cloning and sequence analysis of flaA, a gene encoding a Spirochaeta aurantia flagellar filament surface antigen [10].
• In this study, hemodynamic function, plasma renin activity (PRA), AII, prostacyclin (PGI2), and thromboxane B2 (TxB2) levels were measured in 17-20-day-old dogs before and 1, 2, and 3 hr after endotoxin administration (1 mg/kg, Escherichia coli lipopolysaccharide-B) [11].

Biological context of fliM

• The Escherichia coli operon designated flaA contains seven flagellar genes; among them are two switch protein genes whose products are believed to interface with the motility and chemotaxis machinery of the cell [12].
• Complementation analysis using several plasmids carrying different portions of the flaA operon and analysis of expression of these plasmids in minicells allowed the identification of two flagellar gene products [12].
• The flaA (cheC) locus from Escherichia coli is important in controlling the rotational direction of flagella during chemotaxis [1].
• The C. crescentus fliL and fliM genes form an operon that is expressed early in the cell cycle [13].
• A frameshift mutation was constructed in the fliM gene, and the mutation was transferred onto the B. subtilis chromosome [2].

Anatomical context of fliM

• No analogs to the bacterial chemotactic and motility (che, mot, fla) genes, genes for a two-component signal transduction system, genes associated with gliding, or genomic homologs for the eukaryotic cytoskeleton and motor proteins were found in the Mollicutes [14].

Associations of fliM with chemical compounds

• Recombinant apoAIV complex with Myr2GroPCho was also able to bind to the same apoAI/AII receptor sites and to promote cholesterol efflux to an equal extent from adipose cells [15].
• Forms AI and AII are separated on a phosphocellulose column, purified by further ion-exchange chromatography, and by sedimentation through a glycerol gradient [16].
• RESULTS: Amplicons bearing 500 or 150 bp flanking regions of flaA on each side (depending on the strain) were sufficient to allow the specific insertion of a 1173 bp chloramphenicol cassette into the genome of H. pylori [17].
• It was found that transcription of genes responsible for the formation and/or function of flagella (hag, fla, mot, che) decreased significantly at 40 degrees C. However, in the ftsI730 mutant at the nonpermissive temperature, or in penicillin G treated wild-type cells, cell division was blocked but formation of flagella continued [18].
• Captopril significantly blunted the rise in PRA and AII, while indomethacin blocked the rise in PGI2 and TxB2 [11].

Regulatory relationships of fliM

• Genetic analysis of Escherichia coli has identified fliG and fliM as genes in which mutations occur that allele specifically suppress cheY mutations, indicating interactions among these gene products [19].

Other interactions of fliM

• There were two possible initiation codons (ATG) for motD translation, the first of which overlapped with the termination codon of the upstream gene, flaAII (fliN) [12].

Analytical, diagnostic and therapeutic context of fliM

• RT-PCR analysis indicated that the chemotaxis genes and the upstream flagellar gene flaA constitute an operon [20].
• An oligonucleotide primer pair from a conserved 5' region of the flaA gene of C. coli VC167 was used to amplify a 450-bp region by PCR [21].
• The Borrelia burgdorferi 37-kilodalton immunoblot band (P37) used in serodiagnosis of early lyme disease is the flaA gene product [22].
• Subjects were assigned to 4 vaccination groups: groups AI, AII, and AIII received intranasal influenza vaccine from batches that differed in the hemagglutinin and neuraminidase strains used, and group B received intramuscular virosomal subunit vaccine [23].
• Captopril may benefit vital organ and tissue perfusion by inhibiting AII formation [24].

References