Disease relevance of fliA

• We have cloned the Escherichia coli fliAZY operon, which contains the fliA gene (the alternative sigma factor sigma F) and two novel genes, fliZ and fliY [1].
• Accordingly, it was thought that the polyhook of the flaD flaE mutant had a mechanical defect for chi phage infection [2].
• We began an analysis of rpoF, the gene encoding the cryptic, 37,000-dalton minor sigma factor (sigma-37) of Bacillus subtilis RNA polymerase [3].

High impact information on fliA

• QseBC activates transcription of flhDC, which is the master regulator for the flagella and motility genes and, in the absence of flhD, QseBC failed to activate the transcription of fliA [4].
• The genes flaD, E, G, H, I and J share high homologies with genes from other Archaea. Interestingly, flaK shows similarities to bacterial genes involved in the regulation of flagellar synthesis [5].
• One involved the arabinose-induced expression of plasmid-encoded sigma(28)(Ct) in a strain of Escherichia coli defective in the sigma(28) structural gene, fliA [6].
• By plasmid integration and PBS1 transduction, we found the chromosomal locus of rpoF linked to ddl and dal at 40 degrees on the B. subtilis map and near no known lesions affecting growth regulation or development [3].
• The DNA sequence also suggested that rpoF may lie in a gene cluster [3].

Biological context of fliA

• Further, an rpoF null mutation resulting from gene disruption had no effect on cell growth or sporulation in rich medium, suggesting that sigma-37 may partly control a regulon not directly involved in the sporulation process [3].
• Immediately following rpoF was a reading frame that would encode a protein of at least 20,000 daltons; expression of this region may be translationally coupled to that of rpoF [3].
• Upstream of rpoF was an open reading frame that would encode a protein of 17,992 daltons; this frame overlapped the rpoF-coding sequence by 41 base pairs [3].
• The integration of a plasmid having chloramphenicol resistance closely linked to the flaD gene into the B. subtilis AC703 chromosome and its genetic analysis indicated that the cloned fragment contained the flaD gene itself [7].

Other interactions of fliA

• The presence of flagella was also found to be important as qseB and fliA mutants (which lack flagella) had less biofilm than the isogenic paralyzed motA strain (threefold less thickness and 15-fold less surface coverage) [8].
• BW25113, MG1655 qseB, and MG1655 fliA had poor biofilms (surface coverage less than 5%) [8].
• This increase in motility due to deleting hha/ybaJ was found to be due to 8-fold induction of fliA transcription [9].

Analytical, diagnostic and therapeutic context of fliA

• Gene fliA was amplified by the polymerase chain reaction, subcloned into expression vector pT7-7, and overexpressed [10].

References