Disease relevance of fliC

• In vivo, fliC expression by Salmonella enterica serovar Typhimurium is heterogeneous, regulated by ClpX, and anatomically restricted [1].

High impact information on fliC

• Furthermore, viable flagellin-deficient mutant organisms (fliC/fljB and flhD) failed to elicit IL-8 secretion when added apically to model intestinal epithelia [2].
• When the fljB-fljA operon is expressed, only type B flagella are produced; when the operon is not transcribed, the gene for type C flagellin (fliC) is released from inhibition and forms type C flagella [3].
• Altered levels of flagellin (fliC), PagC, IroN, and outer membrane proteins suggest that the slyA mutation affects the surface properties of Salmonella [4].
• The intracellularly transcribed pagC promoter was upregulated by Salmonella in all tissues, defining the infected PP as a unique environment that initiates expression of intracellularly induced genes and yet permits transcription of fliC [1].
• Here, we use flow cytometry to quantify fliC gene expression in single bacteria [1].

Biological context of fliC

• This identified a predicted stem-loop structure, SL2, as an effector of normal fliC mRNA translation [5].
• Second-site suppressors that restored fliC translation and motility included mutations that disrupt a RNA duplex stem formed between RNA sequences in the fliC 5'UTR SL2 region (including a precise deletion of SL2) and bases early within the fliC-coding region [5].
• In a previous study we used targeted mutagenesis of the 5' end of the fliC gene to isolate single base changes defective in fliC gene translation [5].
• Primer extension mapping determined the transcription start site of the fliC flagellin gene to be 62 bases upstream of the AUG start codon [6].
• Single base changes defective in translation were located in three regions: the AUG start codon, the presumed ribosomal binding site region, and a region near the very 5' end of the fliC mRNA that corresponded to a potential stem-loop structure in the 5'UTR [6].

Anatomical context of fliC

• In orally infected mice, fliC transcription was anatomically restricted: Salmonella transcribed fliC in the Peyer's Patches (PP) but not in the mesenteric lymph nodes and spleen [1].
• InvA, which is essential for Salmonella spp. to enter cultured epithelial cells, is a member of a family of proteins involved in either flagellar biosynthesis or the secretion of virulence determinants by a number of plant and mammalian pathogens [7].

Other interactions of fliC

• The serT allele causes a 10-fold increase in sigma(28)-dependent fliC promoter transcription, indicating a defect in FlgM anti-sigma(28) activity in the presence of the serT mutation [8].
• At 20 min after induction, the class 2 fliA promoter became active and intracellular FliA protein levels increased; at 30 min after induction, the class 3 fliC promoter was activated [9].
• In this study, overlapping recombinant flagellin fragments were constructed from the fliC (H:i) and fljB (H:1,2) flagellin genes, and the expression products were tested for binding to H antigen-specific monoclonal and polyclonal antibodies [10].
• In phase-2 cells of diphasic Salmonella strains, expression of the phase-1 flagellin-encoding gene, fliC, is repressed by the repressor encoded by the fljA gene [11].

Analytical, diagnostic and therapeutic context of fliC

• Northern blotting analysis revealed that no fliC mRNA was detected in phase 2 cells [12].
• Sequence analysis of operator mutants of the phase-1 flagellin-encoding gene, fliC, in Salmonella typhimurium [11].

References