Disease relevance of ftsQ

• A 1.2-kilobase-pair BamHI fragment from a cell envelope-cell division gene cluster of Escherichia coli containing ddl and part of ftsQ was cloned and sequenced, and the sequence was interpreted with the aid of genetic complementation and promoter fusion data for the region [1].
• We have used the easily synchronizable bacterium Caulobacter crescentus to determine when the cell division genes ftsQ and ftsA are transcribed during the DNA replication cycle and to compare their transcription with that of ftsZ [2].
• The three ORFs (YFIH, ORF5 and ORF6) located downstream of the cell division genes ftsQ and ftsZ in Brevibacterium lactofermentum were disrupted by single homologous recombination events between internal fragments of the corresponding genes and the chromosomal sequences [3].

High impact information on ftsQ

• The ftsQA genes, which encode functions required for cell division in E. coli, are regulated by promoters P1 and P2, located upstream of the ftsQ gene [4].
• The promoter, ftsA1p, located in the ftsQ coding sequence, co-regulates ftsA and ftsZ [5].
• Cells which are lysogenic for lambda JFL100 transcribe the cloned lacZ from promoter(s) within the ftsQ and ftsA sequences [6].
• Here we also describe a novel screen for cell division mutants based on a wrinkled-colony morphology, which yielded several new point mutations in ftsQ [7].
• In ftsA, ftsI, and ftsQ mutants, which form filaments with an indented morphology, Z rings formed but their contraction was blocked [8].

Biological context of ftsQ

• Whereas the latter strains showed a slow recovery of cell division after a shift back to the permissive temperature, ftsZ and ftsQ filaments recovered quickly [9].
• Analysis of the DNA sequence further showed that the termination codon of ddl is separated from the initiation codon of ftsQ by one base, which suggests that these two genes may be translationally coupled when transcription is initiated upstream of ddl [1].
• The analysis revealed defective ftsQ and mraY genes, truncated by a nonsense and a frame-shift mutation, respectively [10].
• The essential cell division genes ftsQ, ftsA and ftsZ map in a cluster of cell envelope genes located at two minutes on the Escherichia coli genetic map and appear to constitute an atypical operon [11].
• Amplification of a 2.6-kilobase chromosomal fragment of the mra region of Escherichia coli encompassing the ftsI(pbpB) gene and an open reading frame upstream with lethal to E. coli strains with mutations of the flanking cell division genes ftsQ, ftsA, and ftsZ [12].

Anatomical context of ftsQ

• 2) The ftsQ and ftsl gene products are integral proteins of the cytoplasmic membrane with small cytoplasmic domains and large periplasmic domains [13].

Associations of ftsQ with chemical compounds

• The ftsQ gene product was identified by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and two-dimensional gel electrophoresis of radiolabeled, isopropyl-beta-D-thiogalactopyranoside-induced maxicell and normal cell extracts [14].

Physical interactions of ftsQ

• The observation that the termination codon of ftsQ overlaps with a potential initiation codon for ftsA suggested that these two genes may be translationally coupled when transcription is initiated upstream of the ftsQ coding sequence [15].

Regulatory relationships of ftsQ

• We have previously shown that ftsA can be expressed from a weak promoter located within the ftsQ gene (Robinson et al., J. Bacteriol. 160:546-555, 1984) [16].

Other interactions of ftsQ

• Already at the premissive temperature, all mutants, particularly the pbpB and ftsQ mutants, showed an increased average cell length and cell mass [9].

Analytical, diagnostic and therapeutic context of ftsQ

• The pbpB and ftsQ mutants also exhibited a prolonged duration of the constriction period [9].
• The upstream flanking region of the ftsQ and ftsZ genes of Brevibacterium flavum MJ233, which belongs to the coryneform bacteria, was amplified by the inverse polymerase chain reaction method and cloned in Escherichia coli [17].
• Semi-quantitative RT-PCR analyses of gfp transcripts driven by cloned MtftsZ promoter regions in M. smegmatis cells showed threefold higher promoter activity from ftsQ ORF than from the ftsQ-ftsZ intergenic region [18].

References