Disease relevance of fliC

• Structural and functional implications of sequence diversity of Pseudomonas aeruginosa genes oriC, ampC and fliC [1].
• We tested the role of flagella in the initial stages of respiratory tract infection by comparing the virulence of fliC mutants in a neonatal mouse model of pneumonia [2].
• In HAECs, PAO1, PAK, and Burkholderia cepacia, but not flagellin-deficient strain PAK/fliC or a B. cepacia fliC mutant, activated the NF-kappaB reporter [3].
• Flagellin gene fliC of Xanthomonas campestris is upregulated by transcription factor Clp [4].

High impact information on fliC

• Unexpectedly, the flhA mutant adhered significantly better to corneal epithelial cells than wild-type bacteria or the fliC mutant did [5].
• Similar Western blot analyses of 50 more P. aeruginosa strains obtained from varied sources revealed that all strains contained either A-type or B-type FliD, suggesting the existence of only two types of FliD in P. aeruginosa and indicating that fliC and fliD were coinherited [6].
• Single point mutations lead to a mean sequence diversity of 0.40%, 0.38% and 0.59% for oriC, ampC and a-type fliC, respectively, but of only 0.05% for b-type flagellin genes [1].
• In the absence of fliC, there was no mortality, compared with 30% mortality attributed to the parental strain PAK or 15% mortality associated with infection due to a pilA mutant PAK/NP (P < 0.0001) [2].
• Fla+ organisms but not fliC mutants were efficiently taken up by murine macrophages [2].

Biological context of fliC

• Physical genome analysis of the virulence-associated fliC locus in 20 Pseudomonas aeruginosa strains by mapping and sequencing revealed groups of heterologous a-type (1164 bp; 1185 bp) and highly conserved b-type (1467 bp) flagellin genes [7].
• The combination of these SNPs plus the type of fliC present (a or b) allowed the assignment of a genetic fingerprint to each strain, thus providing a simple tool for the discrimination of P. aeruginosa strains [8].
• Cloning and comparison of fliC genes and identification of glycosylation in the flagellin of Pseudomonas aeruginosa a-type strains [9].
• Surprisingly, by using a reporter gene fusion with the fliC promoter (pfliC::xylE), it was found that fliC expression begins within hours of static growth and is reversible after returning the culture to shaking conditions [10].

Anatomical context of fliC

• Nutrient-induced biofilm dispersion was associated with increased expression of flagella (fliC) and correspondingly decreased expression of pilus (pilA) genes in dispersed cells [11].
• To determine which TLRs mediate recognition of P. aeruginosa, we measured cytokine responses of bone marrow cells from wild-type mice and mice lacking TLR2 (TLR2(-/-)), TLR4 (TLR4(-/-)), TLR2 and TLR4 (TLR2/4(-/-)), or MyD88 (MyD88(-/-)) to wild-type P. aeruginosa and to fliC P. aeruginosa, which lacks the TLR5 ligand flagellin [12].

Other interactions of fliC

• The fbp gene (28 to 29 min), which encodes an outer membrane ferripyochelin-binding protein of low molecular weight, and the fliC gene (64 to 66 min), the flagellin structural gene, were determined to lie in the previously reported locations [13].
• AlgT-dependent control of flagellum synthesis occurred through inhibition of fliC but not rpoN transcription [14].
• The majority of isolates (59%) were PCR-positive for exoU rather than for exoS (38%), and carried a-type fliC genes (76%) rather than b-type (24%) [15].

Analytical, diagnostic and therapeutic context of fliC

• Sequence analysis of three representative gene loci, oriC, ampC and fliC, in 19 Pseudomonas aeruginosa strains revealed a low sequence diversity that does not correlate with the extensive diversity of P. aeruginosa habitats [1].

References