Disease relevance of fliA

• Late gene expression during flagellum biosynthesis in Salmonella typhimurium is dependent upon an alternative sigma factor, sigma28, the product of the fliA gene [1].
• Remarkably the fliA gene from the extreme thermophile Aquifex aeolicus restored motility to the E. coli mutant at relatively low temperature, albeit partially [2].

High impact information on fliA

• Using a set of fliA deletion mutants in a high-expression plasmid, we demonstrated that polypeptides containing the C-terminal portion of FliA could titrate the intracellular FlgM protein resulting in derepression of the class 3 operons [3].
• The V. cholerae genome sequence revealed the presence of a fliA gene, which is predicted to encode the alternative flagellar sigma factor sigma28 [4].
• 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 [5].
• Transcription of the late (Class 3) flagellar promoters in Salmonella typhimurium is dependent upon the flagellar specific sigma factor, sigma28, encoded by the fliA gene. sigma28-dependent transcription is inhibited by an anti-sigma factor, FlgM, through a direct interaction [6].
• We found that serovar Typhi strains carrying a null mutation in either of the flagellar regulatory genes flhDC or fliA were severely deficient in entry into cultured epithelial cells and macrophage cytotoxicity [7].

Biological context of fliA

• The class 3 operons are controlled positively by fliA and negatively by flgM [8].
• Thus, fatty acid derivatives may act as intracellular signals to regulate hilA expression. flhDC and fliA encode transcription factors required for flagellum production, motility, and chemotaxis [9].
• Mutation of flgM attenuates virulence of Salmonella typhimurium, and mutation of fliA represses the attenuated phenotype [10].
• The nucleotide sequence downstream of the fliA gene was determined [11].
• The sequence contains two ORFs following the fliA gene [11].

Anatomical context of fliA

• However, a flgM-fliA double mutant was fully virulent in mice and survived in macrophages at wild-type levels [10].

Other interactions of fliA

• However, though neither flhD nor flhC mutants could express the class 2 operons, the fliA mutants permitted the basal-level expression of those operons [8].

References