Disease relevance of recF

• Transcriptional organization of the dnaN and recF genes of Escherichia coli K-12 [1].
• Sequence and complementation analysis of recF genes from Escherichia coli, Salmonella typhimurium, Pseudomonas putida and Bacillus subtilis: evidence for an essential phosphate binding loop [2].
• We have compared the recF genes from Escherichia coli K-12, Salmonella typhimurium, Pseudomonas putida, and Bacillus subtilis at the DNA and amino acid sequence levels [2].
• To do this we determined the complete nucleotide sequence of the recF gene from Salmonella typhimurium and we completed the nucleotide sequence of recF gene from Pseudomonas putida begun by Fujita et al [2].
• recF in Actinobacillus pleuropneumoniae [3].

High impact information on recF

• Mutations in recF, recO or recR gene abolish induced mutagenesis in E. coli [4].
• Stationary phase induction of dnaN and recF, two genes of Escherichia coli involved in DNA replication and repair [5].
• Our results suggest that stationary phase-dependent mechanisms have evolved in order to coordinate expression of dnaN and recF independently of the dnaA regulatory region [5].
• After UV-induced DNA damage in Escherichia coli, RecA and several recF pathway proteins are thought to process arrested replication forks and ensure that replication resumes accurately [6].
• Properties of a mutant recA-encoded protein reveal a possible role for Escherichia coli recF-encoded protein in genetic recombination [7].

Chemical compound and disease context of recF

• Regulatory role of recF in the SOS response of Escherichia coli: impaired induction of SOS genes by UV irradiation and nalidixic acid in a recF mutant [8].

Biological context of recF

• These results indicate that the dnaN and recF genes are organized in an operon [1].
• However, a deletion inactivating dnaN without changing the reading frame of the gene does not affect expression of the recF gene [1].
• An open reading frame of 1071 base pairs has been identified with the recF structural gene [9].
• The results suggest that recF plays a regulatory role in the SOS response [8].
• N-terminal protein sequence analysis demonstrated that the purified protein had the sequence that was predicted from the DNA sequence of the recF gene, except that the predicted N-terminal Met was not present [10].

Associations of recF with chemical compounds

• The results suggest that the streptomycin-resistant transformants arise exclusively via a recombinational pathway which is largely dependant on the recF gene product, and that this pathway is influenced by induction of the SOS response [11].
• We have located the single nucleotide changes suffered in recA sequence of 2 recF partial suppressor mutations: srf-2020 at codon 121 and srf-801 at codon 257. srf-2020 changes codon 121 from threonine (ACC) to isoleucine (ATC). srf-801 changes codon 257 from glutamine (CAG) to proline (CCG) [12].
• This uninduced mutagenesis is independent of the umuC+, recF+ and recA+ genes and we hypothesize that it is regionally targeted on pyrimidine cyclobutane or 6-4 dimers in the vicinity of the target CTC and GAG nucleotides [13].
• Thus, we conclude that the induced (umuC and recF dependent) mutagenesis is locally targeted on pyrimidine cyclobutane or 6-4 dimers. glyU carried by M13 is equally subject to uninduced UV mutagenesis whether carried by mp8 or mp9 [13].

Regulatory relationships of recF

• When carried by M13 phage mp9, glyU is subject to induced UV mutagenesis which is dependent on the umuC+ and recF+ genes [13].

Other interactions of recF

• The low level of transcription coming to the end of recF, and the highest activity of the gyrB promoter, as well as results obtained with several gyrB::lacZ translational fusions, support the conclusion that gyrB is predominantly expressed from its own promoter under standard growth conditions [14].
• recF-dependent and recF recB-independent DNA gap-filling repair processes transfer dimer-containing parental strands to daughter strands in Escherichia coli K-12 uvrB [15].
• The level of translation of recF-lacZ fusions is reduced 20-fold by nucleotides 49 to 146 of recF [16].
• However, no synergistic interactions were discovered between recG258 and mutations in recF, recN, or recQ [17].
• This in turn led to the discovery of several genes, including recF, recO, and recR, whose role in recombination would not otherwise have been detected [18].

References