Disease relevance of F Factor

• The most significant feature in this regard may be the lack of a region of dyad symmetry within the presumptive promoter of the F plasmid ssf gene as is found in the region of the presumptive E. coli ssb promoter [1].
• A purified EcoRI restriction endonuclease fragment that determines resistance to kanamycin and is incapable of self-replication was used to select autonomously replicating fragments from an EcoRI digest of a Salmonella typhimurium F' plasmid containing the chromosomal region believed to include the S. typhimurium origin of DNA replication [2].
• The single-stranded DNA-binding proteins from bacteriophage T4, F plasmid, Escherichia coli, and calf thymus can all be covalently cross-linked in vitro to thymine oligonucleotides by irradiating the respective protein-oligonucleotide complexes with ultraviolet light [3].
• Repression of the virulence of Yersinia pestis by an F' plasmid [4].
• Thus, as the influenza C glycoprotein is the only myxovirus glycoprotein with three different activities, we propose the designation HEF in order to describe its function as a haemagglutinin (H), an esterase (E) and a fusion factor (F) [5].

High impact information on F Factor

• Derived from the leading region of F plasmid, single-stranded Frpo sequence directs RNA polymerase to initiate transcription at a specific site within Frpo, and this specific transcription is highly stimulated by SSB [6].
• This strain carries a revertible mutant lac allele on an F plasmid and accumulates Lac+ (lactose utilizing) revertants, but not unselected mutants, when placed on selective medium [7].
• The anticoagulant effect of short heparin chains, including the minimal AT-specific pentasaccharide, is mediated exclusively through the allosteric activation of AT towards efficient inhibition of coagulation factors (f) IXa and Xa [8].
• The protein FinO represses F-plasmid conjugative transfer by facilitating interactions between the mRNA of the major F-plasmid transcriptional activator, TraJ, and an antisense RNA, FinP [9].
• It is plausible that the near polar localization of SopB may serve the function of keeping a segregated pair of F plasmids apart while the cell septum is being formed [10].

Chemical compound and disease context of F Factor

• Hfr strains that carry the F factor adjacent to argF (one of two duplicate genes that code for ornithine transcarbamylase in E. coli K12) yield more Cut mutants than do F+ or F- strains, or Hfr strains in which the F factor is not adjacent to argF [11].
• Several F' plasmids encoding resistance to tetracycline have been derived from a trg::Tn10 Hfr B7 strain of Escherichia coli K-12 [12].
• The aberrantly regulated dihydrofolate reductase gene mediating trimethoprim resistance could be transduced into E. coli K-12 or moved by recombination into an F' factor and then transferred into trans position in relation to the corresponding chromosomal gene [13].
• Sixty-two E. coli mutants, selected as being deficient as recipients in F factor conjugation, are altered either in the amount or function of the outer membrane OmpA protein or in lipopolysaccharide structure [14].

Biological context of F Factor

• The drug-resistance plasmid, NR1, is a 37-micron circular DNA molecule that contains two components: the resistance transfer factor (29 micron) carrying the transfer genes and the genes for tetracycline resistance, and the r-determinant (8 micron) carrying the genes for resistance to several other antibiotics including chloramphenicol (Cm) [15].
• In Escherichia coli K-12 strains that carry the mutation ssb-1 in the gene for single-stranded DNA binding protein, the presence of the F sex factor partially reverses the temperature-sensitive growth phenotype caused by the mutation [16].
• Dispensable replicons such as F plasmid [95 kilobases (kb)] or its mini-derivatives such as mini-F (9.3 kb) or lambda mini-F efficiently induced cellular SOS genes such as sfiA (sulA) when they were damaged by UV irradiation and then introduced into a recipient bacterium [17].
• We have determined the sequence of the gene encoding a single-stranded DNA (ss DNA) binding protein (SSB) from the Escherichia coli F sex factor and the amino acid sequence of the protein it encodes [1].
• Recently, molecular genetic studies have suggested that DNA helicase I, which is known to be encoded on the F plasmid, may be involved in this nicking reaction (Traxler, B. A., and Minkley, E. G., Jr. (1988) J. Mol. Biol. 204, 205-209) [18].

Anatomical context of F Factor

• The different functional complexes of ribosomes with elongation factor F (EF-G) were studied by digestion experiments with trypsin [19].
• Due to the reported lack of factor (F) X in semen, it has been suggested that TF may not have a role in seminal coagulum formation [20].
• Monocytes synthesize factor (F) XIII, implying that FXIII (a and s) in synovial tissue might help to differentiate between RA and OA [21].
• Thus, correlations between the peroxidation level, superoxide dismutase (SOD) activity, antioxidant factor (F), and indexes of resistance of erythrocytes for hemolysis (TR) were found [22].

Associations of F Factor with chemical compounds

• Steroid/nuclear hormone receptors are ligand-regulated transcription f factors that play key roles in cell regulation, differentiation, and oncogenesis [23].
• The protein cofactor, factor (F) VIIIa, is required for the efficient conversion of the substrate FX to FXa by the serine protease FIXa [24].
• Transfer of all three plasmids was affected differently by mutations in the rfa (LPS) locus of the recipient cell, the F plasmid being most sensitive to mutations that affected rfaP gene expression which is responsible for the addition of pyrophosphorylethanolamine (PPEA) to heptose I of the inner core of the LPS [25].
• ColB2 transfer was more strongly affected by mutations in the heptose II-heptose III region of the LPS (rfaF) whereas R100-1 was not strongly affected by any of the rfa mutations tested. ompA but not rfa mutations further decreased the mating efficiency of an F plasmid carrying a mutation in the mating-pair stabilization protein TraN [25].
• Genetic factors affecting recovery of nonpoint mutations in the region of a gene coding for ornithine transcarbamylase: involvement of both the F factor in its chromosomal state and the recA gene [11].

Gene context of F Factor

• When a chimeric construct between pBR322 and pSC101 was introduced into a polA rnh double mutant, the replication of the plasmid via the pBR322 replicon was inhibited if the plasmid also carried an rnh+ gene or if the host harbored an F' plasmid carrying an rnh+ gene [26].
• Using a traD overexpression plasmid, we purified the F sex factor TraD protein in milligram quantities [27].
• Protein Z-dependent protease inhibitor (ZPI) is a serpin inhibitor of coagulation factor (F) Xa dependent on protein Z, Ca2+, and phospholipids [28].
• srnB is an F-plasmid encoded gene, otherwise silent, whose expression is induced by added rifampicin, leading to the release of cellular Mg2+ and degradation of stable RNA [29].
• The F sex factor also carries a psiB gene homologous to that of R6-5 [30].

Analytical, diagnostic and therapeutic context of F Factor

• Escherichia coli DNA helicase I catalyzes a sequence-specific cleavage/ligation reaction at the F plasmid origin of transfer [31].
• Purification, circular dichroism analysis, crystallization and preliminary X-ray diffraction analysis of the F plasmid CcdB killer protein [32].
• Partner switching mechanisms in inactivation and rejuvenation of Escherichia coli DNA gyrase by F plasmid proteins LetD (CcdB) and LetA (CcdA) [33].
• By using F' plasmids carrying different parts of the polA gene, a series of complementation tests was carried out to investigate the requirement for the three enzymatic activities, polymerization, 3'-->5' exonuclease, and 5'-->3' exonuclease activities, of DNA PolI [34].
• After treatment with factor (F) VIII concentrate a significant number of patients with hemophilia A develop inhibitory antibodies that neutralize FVIII [35].

References