Disease relevance of fliL

• Early Caulobacter crescentus genes fliL and fliM are required for flagellar gene expression and normal cell division [1].
• Sequence of the flaA (cheC) locus of Escherichia coli and discovery of a new gene [2].
• We infected various nonflagellated mutants of Escherichia coli with fla-transducing phages and followed the kinetics of the appearance of motility [3].
• Genetic analysis of three additional fla genes in Salmonella typhimurium [4].
• A set of the periodically regulated flagellar (fla) genes of Caulobacter crescentus contain conserved promoter sequence elements at -24 and -12 that are very similar to the sequence of the nitrogen assimilation (Ntr) and nitrogen fixation (Nif) promoters of enteric bacteria and Rhizobium spp [5].

High impact information on fliL

• However, B. subtilis contains several chemotaxis genes not found in the E. coli genome, such as cheC and cheD, indicating that the B. subtilis chemotactic system is more complex [6].
• The deletion strain lacks motility and belongs to the fla(-) mutant class, indicating that it is deficient in flagellar biogenesis [7].
• The fla gene cluster is involved in the biogenesis of flagella in Halobacterium salinarum [7].
• Region I was shown to include at least 12 fla cistrons [8].
• The timing of fla gene expression in the cell cycle is determined by specialized forms of RNA polymerase and the appearance and/or activation of regulatory proteins [9].

Chemical compound and disease context of fliL

• Our results help to define the features of the Ntr/Nif-type consensus sequence required for promoter utilization by purified E. coli E sigma 54 and support the idea that C. crescentus may contain a specialized polymerase with similar promoter specificity required for expression of a set of fla genes [5].

Biological context of fliL

• The C. crescentus fliL and fliM genes form an operon that is expressed early in the cell cycle [1].
• The flaA (cheC) locus from Escherichia coli is important in controlling the rotational direction of flagella during chemotaxis [2].
• Loss of the flaAI gene product resulted in a nonmotile and nonflagellated phenotype [10].
• The wild-type flaAI gene on the chromosome was replaced with a flaAI gene mutated in vitro [10].
• A spontaneous fliL mutant of S. typhimurium, containing a frameshift mutation about 40% from the 3' end of the gene, was moderately motile but swarmed poorly, suggesting that FliL might be a component of the flagellar motor or switch [11].

Anatomical context of fliL

• 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 [12].

Associations of fliL with chemical compounds

• The tumbling of cheB or cheE mutants was depressed after prolonged methionine starvation in the presence of a constant level of an attractant. cheC tumbling mutants appeared unique in that they did not cease tumbling even when cells were deprived of methionine [13].
• 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 [14].

Analytical, diagnostic and therapeutic context of fliL

• The engineered apo AI polypeptides were isolated and purified by affinity chromatography and assayed for their activator activity [15].
• We therefore used the method of site-directed mutagenesis of apo AI cDNAs using the overlap extension approach by the polymerase chain reaction [15].

References