Disease relevance of recO

• Mutations in recF, recO or recR gene abolish induced mutagenesis in E. coli [1].
• Analysis of the Bacillus subtilis recO gene: RecO forms part of the RecFLOR function [2].

High impact information on recO

• The recO gene product is required for RecF pathway-mediated recombination and the repair of DNA damage after UV irradiation or mitomycin C exposure in Escherichia coli [3].
• Mutation of recF, recO or recQ produced recombinants in which this exchange tended to be closer to the origin, though the effect observed was rather small [4].
• The recO gene product is required for DNA repair and some types of homologous recombination in wild-type Escherichia coli cells [5].
• The recO open reading frame contained three possible translation start codons and could potentially encode a polypeptide of Mr 26,000 [6].
• A combination of deletion mapping and insertional mutagenesis localized the recO-complementing region to an approximately 1-kilobase region of a 1.6-kilobase BamHI fragment [6].

Biological context of recO

• Consistent with this interpretation was the observation that the cpeA mutant phenotype was less pronounced in recF, recJ and recO mutants [7].
• The DNA sequence of the 1.6-kilobase BamHI fragment was determined and contained part of era and a 726-base-pair recO open reading frame [6].
• Polarity studies showed that rnc is in an operon with two other genes, era and recO [8].
• While the plasmid carrying a Ptac promoter failed to overproduce RecO, the plasmid carrying a T7O10 promoter overproduced RecO in large quantity, indicating that the natural recO may be overexpressed [9].

Other interactions of recO

• The results of these studies suggest that recombinational-repair genes, particularly recF, sbcB and recO have different roles in the induced excision of Tn10 than in recombinational mating [10].
• Several lines of evidence suggest that the recF, recO, and recR genes function at the same step of recombination and postreplication repair [11].
• The recO mutation did not affect intramolecular recombination in the addAB, recU, recF or recL cells, but reduced it by about 75-fold in recH cells [2].

Analytical, diagnostic and therapeutic context of recO

• N-Terminal protein sequence analysis of the overexpressed 31 kDa polypeptide confirmed that this polypeptide was encoded by the recO gene [3].
• A combination of primary sequence analysis and secondary structure predictions suggested that recO contains a mononucleotide-binding fold [6].
• In this work, the structural portion of recO was synthesized by the polymerase chain reaction (PCR) and cloned onto expression vectors at their Nco1 fusion cloning site, to eliminate the presence of mRNA leader sequence [9].

References